Journal articles: 'Atherosclerosis Drugs'

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Udupa, S. L. "Indigenous drugs and atherosclerosis." Drugs of Today 37, no. 1 (2001): 37. http://dx.doi.org/10.1358/dot.2001.37.1.608780.

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Orekhov, Alexander N., Gregory N. Baldenkov, Vladimir V. Tertov, Li Hwa Ryong, Sergei G. Kozlov, Anatoly A. Lyakishev, Vsevolod A. Tkachuk, Michael Ya Ruda, and Vladimir N. Smirnov. "Cardiovascular Drugs and Atherosclerosis." Journal of Cardiovascular Pharmacology 12, Supplement 6 (1988): S66—S68. http://dx.doi.org/10.1097/00005344-198812006-00017.

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Bruikman, Caroline S., Robert M. Stoekenbroek, G. Kees Hovingh, and John P. Kastelein. "New Drugs for Atherosclerosis." Canadian Journal of Cardiology 33, no. 3 (March 2017): 350–57. http://dx.doi.org/10.1016/j.cjca.2016.09.010.

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Cao, Qi, Jiarui Zhao, Maochen Xing, Han Xiao, Qian Zhang, Hao Liang, Aiguo Ji, and Shuliang Song. "Current Research Landscape of Marine-Derived Anti-Atherosclerotic Substances." Marine Drugs 18, no. 9 (August 25, 2020): 440. http://dx.doi.org/10.3390/md18090440.

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Atherosclerosis is a chronic disease characterized by lipid accumulation and chronic inflammation of the arterial wall, which is the pathological basis for coronary heart disease, cerebrovascular disease and thromboembolic disease. Currently, there is a lack of low-cost therapeutic agents that effectively slow the progression of atherosclerosis. Therefore, the development of new drugs is urgently needed. The research and development of marine-derived drugs have gained increasing interest from researchers across the world. Many marine organisms provide a rich material basis for the development of atherosclerotic drugs. This review focuses on the latest technological advances in the structures and mechanisms of action of marine-derived anti-atherosclerotic substances and the challenges of the application of these substances including marine polysaccharides, proteins and peptides, polyunsaturated fatty acids and small molecule compounds. Here, we describe the theoretical basis of marine biological resources in the treatment of atherosclerosis.

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Moubayed, Sami P., Therese M. Heinonen, and Jean-Claude Tardif. "Anti-inflammatory drugs and atherosclerosis." Current Opinion in Lipidology 18, no. 6 (December 2007): 638–44. http://dx.doi.org/10.1097/mol.0b013e3282f0ee11.

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Evangeline, Seth, and Priya R. Iyer. "Atherosclerosis: Causes and Cures." Healthcare Review 2, no. 1 (August 5, 2021): 34–44. http://dx.doi.org/10.47285/hr.v2i1.87.

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Atherosclerosis is a systemic disease that occurs due to the formation of Fibro-fatty lesions in arteries that block blood flow. The process of Atherosclerosis is initiated through mechanical, chemical, and immunological activation of the endothelium. Even there are microorganisms involved in the different stages of atherosclerosis. There are a number of molecular factors, RNA’s, macrophages and enzymes that play a vital role in the progression and development of Atherosclerosis that alter the metabolism of Fibro-fatty. Receptors of micro RNA proliferate and regulate endothelial activation and smooth cell Macrophages, monocytes, t-cell and natural killer cells involved in the boosting of the immune system to prevent the atherosclerotic lesion formation. In this review, we can know how RNA’s involved in the pathophysiology side of atherosclerosis and explore the mechanism to regulate Atherosclerosis, and how macrophages evoke an immune response. Therefore, the use of synthetic and natural drugs and following the right diet timely prevent and reduce the risk of development of Atherosclerosis.

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Boskovic, Srdjan, and Aleksandar Neskovic. "Atherosclerosis plaque regression." Medical review 59, no. 1-2 (2006): 38–45. http://dx.doi.org/10.2298/mpns0602038b.

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Introduction. The natural history of atherosclerosis can be assessed using different methods including quantitative coronary angiography, intravascular ultrasound, B-mode ultrasound, electron-beam computed tomography and magnetic resonance imaging. Regression of atherosclerosis. Although the first investigations regarding effects of low cholesterol diet on atherosclerosis progression in animals were performed almost 100 years ago, researches on potential induction of atherosclerosis regression in humans began only recently, in the past 20 years. To date, many studies assessing different drugs and study protocols on natural evolution of atherosclerosis have been performed. They include use of diet and physical activity, different hypolipemic drugs, especially statins, ACE inhibitors, calcium channel blockers, hormone replacement therapy, antioxidants, and recently, use of recombinant apolipoproteins. Statins and atherosclerosis. It has been established that statins given to patients with, or even without verified coronary artery disease, slow progression of atherosclerosis. These effects of statins are likely due to a combination of their metabolic and pleiotropic properties and might in part explain the positive effects of these drugs on overall cardiovascular mortality and morbidity. Furthermore, applied in high doses, these drugs may induce real atherosclerosis regression, especially in asymptomatic patients in the early stages of the disease. .

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Skripnikova, I. A., O. V. Kosmatova, M. A. Kolchinа, M. A. Myagkova, and N. A. Alikhanova. "Atherosclerosis and Osteoporosis. Common Targets for the Effects of Cardiovascular and Anti-Osteoporotic Drugs (Part II). The Effect of Antiosteoporotic Drugs on the Vascular Wall State." Rational Pharmacotherapy in Cardiology 15, no. 3 (July 6, 2019): 359–67. http://dx.doi.org/10.20996/1819-6446-2019-15-3-359-367.

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In the second part of the literature review, data are presented on the possible effect of anti-osteoporosis therapy on the vascular wall and the development of calcification. The discovery of common biological substances involved in the development of atherosclerosis, calcification of the vascular wall and osteoporosis attracts the attention of scientists in terms of targets for assessing the effects of already known drugs or developing new drugs that can simultaneously prevent or slow the progression of both atherosclerosis and osteoporosis. Currently, various groups of drugs for the treatment of osteoporosis have been studied to prevent or reduce the progression of subclinical atherosclerosis and calcification. Both antiresorptive drugs (bisphosphonates, monoclonal antibodies to RANKL, selective estrogen receptor modulators), and bone-anabolic therapy, which includes teriparatide, were studied. However, there are a few such studies and the most promising drugs that have a preventive effect in the early stages of atherosclerotic damage are bisphosphonates. Other classes of antiosteoporotic drugs did not reveal a positive effect on the vascular wall, and some of them increased the cardiovascular risk. Divergences in the results of experimental and clinical studies attract attention. If in the experiment almost all drugs for the treatment of osteoporosis had an atheroprotective effect and suppressed vascular calcification, then in clinical conditions only bisphosphonates confirmed the positive effect on the vascular wall.

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Berman, Jeremy P., Michael E. Farkouh, and Robert S. Rosenson. "Emerging anti-inflammatory drugs for atherosclerosis." Expert Opinion on Emerging Drugs 18, no. 2 (May 16, 2013): 193–205. http://dx.doi.org/10.1517/14728214.2013.801453.

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Gallego-Colon, Enrique, Wojciech Wojakowski, and Tomasz Francuz. "Incretin drugs as modulators of atherosclerosis." Atherosclerosis 278 (November 2018): 29–38. http://dx.doi.org/10.1016/j.atherosclerosis.2018.09.011.

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Makheja, A. N., S. Bloom, R. Muesing, T. Simon, and J. M. Bailey. "Anti-inflammatory drugs in experimental atherosclerosis." Atherosclerosis 76, no. 2-3 (April 1989): 155–61. http://dx.doi.org/10.1016/0021-9150(89)90099-3.

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Mo, Huaqiang, Chenxing Fu, Zhiye Wu, Peng Liu, Zhibo Wen, Qingqing Hong, Yanbin Cai, and Gongxin Li. "IL-6-targeted ultrasmall superparamagnetic iron oxide nanoparticles for optimized MRI detection of atherosclerotic vulnerable plaques in rabbits." RSC Advances 10, no. 26 (2020): 15346–53. http://dx.doi.org/10.1039/c9ra10509c.

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Herein, we report Anti-IL-6-USPIO for detecting IL-6 in inflammatory macrophages and MR imaging vulnerable plaques of atherosclerosis in rabbit, which would provide a novel non-invasive strategy for evaluating acute cardiovascular risk or exploiting anti-atherosclerotic drugs.

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Kypreos, Kyriakos E., Rafael Bitzur, Eleni A. Karavia, Eva Xepapadaki, George Panayiotakopoulos, and Caterina Constantinou. "Pharmacological Management of Dyslipidemia in Atherosclerosis: Limitations, Challenges, and New Therapeutic Opportunities." Angiology 70, no. 3 (June 3, 2018): 197–209. http://dx.doi.org/10.1177/0003319718779533.

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Clinical and epidemiological studies during the last 7 decades indicated that elevated low-density lipoprotein cholesterol (LDL-C) levels and reduced high-density lipoprotein cholesterol (HDL-C) levels correlate with the pathogenesis and progression of atherosclerotic lesions in the arterial wall. This observation led to the development of LDL-C-lowering drugs for the prevention and treatment of atherosclerosis, some with greater success than others. However, a body of recent clinical evidence shows that a substantial residual cardiovascular risk exists even at very low levels of LDL-C, suggesting that new therapeutic modalities are still needed for reduction of atherosclerosis morbidity and mortality. Unfortunately, HDL-C-raising drugs developed toward this goal had disappointing results thus far. Here, we critically review the literature presenting available evidence and challenges that need to be met and discuss possible new avenues for the development of novel lipid pharmacotherapeutics to reduce the burden of atherosclerosis.

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Reiss, Allison B., Andrew Silverman, Muhammed Khalfan, Nicholas A. Vernice, Lora J. Kasselman, Steven E. Carsons, and Joshua De Leon. "Accelerated Atherosclerosis in Rheumatoid Arthritis: Mechanisms and Treatment." Current Pharmaceutical Design 25, no. 9 (July 9, 2019): 969–86. http://dx.doi.org/10.2174/1381612825666190430113212.

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Background:Rheumatoid arthritis (RA) is a chronic systemic autoimmune inflammatory disorder that increases the risk of developing cardiovascular disease. There is accumulating evidence that the RA disease state accelerates the formation of atherosclerotic plaques. Treatments for RA improve joint symptomatology and may reduce inflammation, but consideration of their effects on the cardiovascular system is generally low priority.Objective:Since cardiovascular disease is the leading cause of mortality in RA patients, the impact of RA therapies on atherosclerosis is an area in need of attention and the focus of this review.Results:The drugs used to treat RA may be analgesics, conventional disease-modifying anti-rheumatic drugs, and/or biologics, including antibodies against the cytokine tumor necrosis factor-α. Pain relievers such as nonselective non-steroidal anti-inflammatory drugs and cyclooxygenase inhibitors may adversely affect lipid metabolism and cyclooxygenase inhibitors have been associated with increased adverse cardiovascular events, such as myocardial infarction and stroke. Methotrexate, the anchor disease-modifying anti-rheumatic drug in RA treatment has multiple atheroprotective advantages and is often combined with other therapies. Biologic inhibitors of tumor necrosis factor-α may be beneficial in preventing cardiovascular disease because tumor necrosis factor-α promotes the initiation and progression of atherosclerosis. However, some studies show a worsening of the lipid profile in RA with blockade of this cytokine, leading to higher total cholesterol and triglycerides.Conclusion:Greater understanding of the pharmacologic activity of RA treatments on the atherosclerotic process may lead to improved care, addressing both damages to the joints and heart.

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Salvamani, Shamala, Baskaran Gunasekaran, Noor Azmi Shaharuddin, Siti Aqlima Ahmad, and Mohd Yunus Shukor. "Antiartherosclerotic Effects of Plant Flavonoids." BioMed Research International 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/480258.

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Atherosclerosis is the process of hardening and narrowing the arteries. Atherosclerosis is generally associated with cardiovascular diseases such as strokes, heart attacks, and peripheral vascular diseases. Since the usage of the synthetic drug, statins, leads to various side effects, the plants flavonoids with antiartherosclerotic activity gained much attention and were proven to reduce the risk of atherosclerosisin vitroandin vivobased on different animal models. The flavonoids compounds also exhibit lipid lowering effects and anti-inflammatory and antiatherogenic properties. The future development of flavonoids-based drugs is believed to provide significant effects on atherosclerosis and its related diseases. This paper discusses the antiatherosclerotic effects of selected plant flavonoids such as quercetin, kaempferol, myricetin, rutin, naringenin, catechin, fisetin, and gossypetin.

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Opar, Alisa. "Where now for new drugs for atherosclerosis?" Nature Reviews Drug Discovery 6, no. 5 (May 2007): 334–35. http://dx.doi.org/10.1038/nrd2326.

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17

JACKSON, R. "Antioxidant drugs for the prevention of atherosclerosis." Journal of Molecular and Cellular Cardiology 23 (April 1991): S35. http://dx.doi.org/10.1016/0022-2828(91)91429-u.

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Paoletti, Rodolfo, Flavia Bruno, and Susanna Colli. "Atherosclerosis and thrombosis. Old and new drugs." Archives of Gerontology and Geriatrics 20, no. 1 (January 1995): 43–48. http://dx.doi.org/10.1016/0167-4943(94)00604-6.

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Rubba, Paolo. "Hypolipidemic drugs on atherosclerosis and arterial function." Pharmacological Research 31 (January 1995): 25. http://dx.doi.org/10.1016/1043-6618(95)86359-1.

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Black, Donald M. "The development of combination drugs for atherosclerosis." Current Atherosclerosis Reports 5, no. 1 (January 2003): 29–32. http://dx.doi.org/10.1007/s11883-003-0065-3.

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Nasonov, E. L., and T. V. Popkova. "Role of interleukin 1 in the development of atherosclerosis." Rheumatology Science and Practice 56 (April 3, 2019): 28–34. http://dx.doi.org/10.14412/1995-4484-2018-28-34.

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Atherosclerosis is now considered as chronic inflammatory vascular disease connected to «pathological» activation of innate and adaptive immunity, characterized by lipid deposition, leukocyte infiltration and proliferation of vascular smooth muscle cells. Subclinical (low grade) inflammation plays fundamental role at all stages of atherosclerotic process progression and determines cardiovascular catastrophes development and mortality. Proinflammatory cytokines including interleukin (IL) 1, IL6, tumor necrosis factor α (TNFα), IL17, IL18, IL27, IL33, IL37 tightly interacting within cytokine network occupy an important place among numerous mediators participating in immunopathogenesis of atherosclerosis and rheumatoid arthritis. IL1β playing an important role in the development of many acute and chronic immunoinflammatory diseases attracts particular attention. IL1β significance in the development of atherosclerosis is determined by many mechanisms including procoagulant activity, enhancement of monocytes and leucocytes adhesion to vascular endothelium, vascular smooth muscle cells growth and others. Fundamental role of inflammation in the development of atherosclerosis is well proved in investigations of anti-atherosclerotic effect of canakinumab. Randomized placebo-controlled trial CANTOS (Canakinumab ANti-inflammatory Thrombosis Otcomes Study) assessing efficacy of canakinumab as new tool for secondary prophylaxis cardiovascular complications in general population of patients with severe atherosclerotic vascular damage. CANTOS results in combination with accumulated in rheumatology data on cardiovascular effects of anti-inflammatory drugs are of great importance for personification of approach to secondary prophylaxis of caused by atherosclerosis cardiovascular complications. They also contribute to the development of inflammatory theory of atherosclerosis pathogenesis in the whole.

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Zagorchev, Lyubomir, and Mary Jo Mulligan-Kehoe. "Advances in imaging angiogenesis and inflammation in atherosclerosis." Thrombosis and Haemostasis 105, no. 05 (2011): 820–27. http://dx.doi.org/10.1160/th10-08-0562.

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SummaryAdvances in imaging technology have provided powerful tools for dissecting the angiogenic and inflammatory aspects of atherosclerosis. Improved technology along with multi-modal approaches has expanded the utilisation of imaging. Recent advances provide the ability to better define structure and development of angiogenic vessels, identify relationships between inflammatory mediators and the vessel wall, validate biological effects of anti-inflammatory and anti-angiogenic drugs, delivery and/or targeting specific molecules to inflammatory regions of atherosclerotic plaques.

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DUTOVA, Svetlana Vyacheslavovna, Julia Vladimirovna SARANCHINA, Oksana Yuryevna KILINA, Nikolai Vladimirovich KHANARIN, and Tatiana Sergeevna KULAKOVA. "MODERN OPPORTUNITIES OF ATHEROSCLEROSIS PHARMACOTHERAPY: NEW DIRECTIONS." Periódico Tchê Química 17, no. 34 (March 20, 2020): 578–90. http://dx.doi.org/10.52571/ptq.v17.n34.2020.602_p34_pgs_578_590.pdf.

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Despite the successful achievements in modern applied medicine and the application of hypolipidemic drugs into clinical practice for the past 50 years, the issue of prevention and treatment of atherosclerotic vascular disease (AVD) remains unsolved. Implementation of the theory of immunopathogenesis of atherosclerosis that was experimentally proved by modern studies allows the specialists to expand the possibilities of pharmacotherapy and pharmacoprevention for AVD. Thus, the aim of the present study was to analyze new directions in the development of anti-atherosclerotic drugs (AAD) with a pathogenetic activity that suppressed chronic autoimmune inflammation in the areas of atherosclerotic damage of vessels. In the course of the study, the search and analysis of the publications in the databases Web of Science, PubMed, and RSCI (Russian Science Citation Index) for the period of 2016-2018 were performed. According to the performed analysis, the most perspective molecular targets for AAD are pro-inflammatory and anti-inflammatory cytokines that develop a disbalance in patients with AVD. Thus, the drugs that are based on monoclonal antibodies to the tumor necrosis factor α (TNFα), and pro-inflammatory interleukins (1β, 17А), used for the treatment of rheumatoid arthritis and psoriasis, can be used for the treatment of AVD. Recombinant interleukins 6, 13, 19, and substances that suppress the expression of interferon regulatory factors will also exert an antiatherogenic effect. The studies on the modeling of the pathogenesis of AVD in inbred animals showed that other molecular targets for AAD could be enzymes involved in the lipid and immune cells metabolism. They include inositol requiring enzyme 1, proprotein convertase subtilisin/Kexin type 9, and the enzymes of paraoxonase family. Besides, the review includes the discussion of the successful application of drugs based on monoclonal antibodies to TNFα (infliximab), IL-17A (secukinumab) and IL-1β (canakinumab), as well as the drugs with antienzymatic activity (evolocumab and darapladib), in clinical practice for the treatment of AVD. The modern knowledge on molecular mechanisms of immunopathogenesis can give grounds for the development of drugs for pathogenetic pharmacotherapy and pharmacoprevention for the complications of AVD. The most effective solution would be the indication of drugs that affect the disbalance of cytokines and metabolic processes in the immune cells.

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Burnett, John R., and Samuel D. Vasikaran. "Cardiovascular disease and osteoporosis: is there a link between lipids and bone?" Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 39, no. 3 (May 1, 2002): 203–10. http://dx.doi.org/10.1258/0004563021902134.

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Atherosclerotic heart disease and osteoporosis are both diseases of old age. Evidence is accumulating for a link between vascular and bone disease. Calcification is a common feature of atherosclerotic plaques, and osteoporosis is associated with both atherosclerosis and vascular calcification. However, the relationship of vascular calcification to the pathogenesis of atherosclerosis remains incompletely understood. Hormone replacement therapy has beneficial effects in the prevention of both atherosclerosis and osteoporosis. Bisphosphonates inhibit bone resorption and are used in the treatment of osteoporosis, whereas the statins inhibit cholesterol biosynthesis and are used for the treatment of atherosclerosis. We have reviewed recent advances in the knowledge of the actions of bisphosphonates and statins at the cellular, molecular and end-organ levels in order to examine the relationship between cardiovascular disease and osteoporosis and to explore the link between lipids and bones. These studies suggest that the mechanism of actions of these two classes of drugs at the cellular level may not be mutually exclusive. There are some early clinical data to complement these findings, suggesting that statins increase bone density and bisphosphonates may have a beneficial effect in vivo on plasma lipid levels and on the atherosclerotic process. Properly designed prospective studies that examine the effect of statins on bone density and fractures, as well as the effects of bisphosphonates on lipid profiles, atherosclerotic progression and cardiovascular morbidity and mortality are needed to define clearly the clinical effects and potential new roles for these agents.

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Talaat, Forayssa M., Tayssir Kamel, Amany M. Rabah, Sandra M. Ahmed, Shaimaa I. El-Jaafary, and Ghada H. Abdelaziz. "Epilepsy and antiepileptic drugs: risk factors for atherosclerosis." International Journal of Neuroscience 125, no. 7 (August 28, 2014): 507–11. http://dx.doi.org/10.3109/00207454.2014.949704.

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Winiarska, Hanna. "Herbal drugs in atherosclerosis prevention – the new evidence." Pharmacological Reports 65 (May 2013): 15–16. http://dx.doi.org/10.1016/s1734-1140(13)71281-7.

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Spanbroek, R., and A. J. Habenicht. "The potential role of antileukotriene drugs in atherosclerosis." Drug News & Perspectives 16, no. 8 (2003): 485. http://dx.doi.org/10.1358/dnp.2003.16.8.829345.

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Stoller, Diane K., Craig B. Grorud, Van Michalek, and Henry Buchwald. "Reduction of Atherosclerosis with Nonsteroidal Anti-Inflammatory Drugs." Journal of Surgical Research 54, no. 1 (January 1993): 7–11. http://dx.doi.org/10.1006/jsre.1993.1002.

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Flierl, Ulrike, and Andreas Schäfer. "Fractalkine – a local inflammatory marker aggravating platelet activation at the vulnerable plaque." Thrombosis and Haemostasis 108, no. 09 (2012): 457–63. http://dx.doi.org/10.1160/th12-04-0271.

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SummaryChemokines play an important role in inducing chemotaxis of cells, piloting white blood cells in immune surveillance and are crucial parts in the development and progression of atherosclerosis. Platelets are mandatory players in the initiation of atherosclerotic lesion formation and are susceptible targets for and producers of chemokines. Several chemokine receptors on platelets have been described previously, amongst them CX3CR1, the receptor for fractalkine. The unique chemokine fractalkine (CX3CL1, FKN) exists as a soluble as well as a membrane-anchored glycoprotein. Its essential role in the formation of atherosclerotic lesions and atherosclerosis progression has been impressively described in mouse models. Moreover, fractalkine induces platelet activation and adhesion via a functional fractalkine receptor (CX3CR1) expressed on the platelet surface. Platelet activation via the FKN/CX3CR1-axis triggers leukocyte adhesion to activated endothelium, and fractalkine-induced platelet P-selectin is mandatory for leukocyte recruitment under arterial flow conditions. This review summarises the role of fractalkine as a potential local inflammatory mediator which influences platelet activation in the setting of atherosclerosis. Beyond that, aspects of a potential interaction between fractalkine and platelet responsiveness to antiplatelet drugs are described. Furthermore, the possible impact of high-density lipoprotein cholesterol (HDL-C) on atherosclerosis progression, platelet activation and fractalkine signalling are discussed.

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Orekhov, Alexander N., Igor A. Sobenin, Victor V. Revin, and Yuri V. Bobryshev. "Development of Antiatherosclerotic Drugs on the basis of Natural Products Using Cell Model Approach." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/463797.

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Atherosclerosis including its subclinical form is one of the key medical and social problems. At present, there is no therapy available for widespread use against subclinical atherosclerosis. The use of synthetic drugs for the prevention of arteriosclerosis in its early stages is not sufficient because of the limited indications for severe side effects and high cost of treatment. Obviously, effective antiatherosclerotic drugs based on natural products would be a preferred alternative. Simple cell-based models for testing different natural products have been developed and the ability of natural products to prevent intracellular lipid accumulation in primary cell culture was evaluated. This approach utilizing cell models allowed to test effects of such direct antiatherosclerotic therapy, analyzing the effects mimicking those which can occur “at the level” of arterial wall via the inhibition of intracellular lipid deposition. The data from the carried out clinical trials support a point of view that the identification of antiatherosclerotic activity of natural products might offer a great opportunity for the prevention and treatment of atherosclerotic disease, reducing cardiovascular morbidity and mortality.

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Zakiev, Emile R., Nikita G. Nikiforov, and Alexander N. Orekhov. "Cell-Based Models for Development of Antiatherosclerotic Therapies." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/5198723.

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The leading cause of death worldwide is cardiovascular disease. Among the conditions related to the term, the most prominent one is the development of atherosclerotic plaques in the walls of arteries. The situation gets even worse with the fact that the plaque development may stay asymptomatic for a prolonged period of time. When it manifests as a cardiovascular disorder, it is already too late: the unfortunate individual is prescribed with a plethora of synthetic drugs, which are of debatable efficacy in the prevention of atherosclerotic lesions and safety. Cell models could be useful for the purpose of screening substances potentially effective against atherosclerosis progression and effective in reduction of already present plaques. In this overview, we present studies making use of in vitro and ex vivo models of atherosclerosis development that can prove valuable for clinical applications.

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Gorabi, Kiaie, Reiner, Carbone, Montecucco, and Sahebkar. "The Therapeutic Potential of Nanoparticles to Reduce Inflammation in Atherosclerosis." Biomolecules 9, no. 9 (August 26, 2019): 416. http://dx.doi.org/10.3390/biom9090416.

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Chronic inflammation is one of the main determinants of atherogenesis. The traditional medications for treatment of atherosclerosis are not very efficient in targeting atherosclerotic inflammation. Most of these drugs are non-selective, anti-inflammatory and immunosuppressive agents that have adverse effects and very limited anti-atherosclerotic effects, which limits their systemic administration. New approaches using nanoparticles have been investigated to specifically deliver therapeutic agents directly on atherosclerotic lesions. The use of drug delivery systems, such as polymeric nanoparticles, liposomes, and carbon nanotubes are attractive strategies, but some limitations exist. For instance, nanoparticles may alter the drug kinetics, based on the pathophysiological mechanisms of the diseases. In this review, we will update pathophysiological evidence for the use of nanoparticles to reduce inflammation and potentially prevent atherogenesis in different experimental models.

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Malekmohammad, Khojasteh, Robert D. E. Sewell, and Mahmoud Rafieian-Kopaei. "Antioxidants and Atherosclerosis: Mechanistic Aspects." Biomolecules 9, no. 8 (July 25, 2019): 301. http://dx.doi.org/10.3390/biom9080301.

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Atherosclerosis is a chronic inflammatory disease which is a major cause of coronary heart disease and stroke in humans. It is characterized by intimal plaques and cholesterol accumulation in arterial walls. The side effects of currently prescribed synthetic drugs and their high cost in the treatment of atherosclerosis has prompted the use of alternative herbal medicines, dietary supplements, and antioxidants associated with fewer adverse effects for the treatment of atherosclerosis. This article aims to present the activity mechanisms of antioxidants on atherosclerosis along with a review of the most prevalent medicinal plants employed against this multifactorial disease. The wide-ranging information in this review article was obtained from scientific databases including PubMed, Web of Science, Scopus, Science Direct and Google Scholar. Natural and synthetic antioxidants have a crucial role in the prevention and treatment of atherosclerosis through different mechanisms. These include: The inhibition of low density lipoprotein (LDL) oxidation, the reduction of reactive oxygen species (ROS) generation, the inhibition of cytokine secretion, the prevention of atherosclerotic plaque formation and platelet aggregation, the preclusion of mononuclear cell infiltration, the improvement of endothelial dysfunction and vasodilation, the augmentation of nitric oxide (NO) bioavailability, the modulation of the expression of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) on endothelial cells, and the suppression of foam cell formation.

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Pęczek, Piotr, Mateusz Leśniewski, Tomasz Mazurek, Lukasz Szarpak, Krzysztof J. Filipiak, and Aleksandra Gąsecka. "Antiplatelet Effects of PCSK9 Inhibitors in Primary Hypercholesterolemia." Life 11, no. 6 (May 23, 2021): 466. http://dx.doi.org/10.3390/life11060466.

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Proprotein convertase subtilisin-kexin type 9 (PCSK9) inhibitors are a novel group of hypolipidemic drugs that are recommended particularly for high-risk hypercholesterolemia patients, including those with primary hypercholesterolemia (PH), where lifelong exposure to high low-density lipoprotein (LDL) cholesterol levels results in an elevated risk of atherosclerosis at an early age. The onset and progression of atherosclerosis is significantly influenced by activated platelets. Oxidized LDL influences platelet activation by interacting with their surface receptors and remodeling the composition of their cell membrane. This results in platelet aggregation, endothelial cell activation, promotion of inflammation and oxidative stress, and acceleration of lipid accumulation in atherosclerotic plaques. PCSK9 inhibitors reduce platelet activation by both significantly lowering LDL levels and reducing the LDL receptor-mediated activation of platelets by PCSK9. They also work synergistically with other hypolipidemic and antithrombotic drugs, including statins, ezetimibe, acetylsalicylic acid, clopidogrel, and ticagrelor, which enhances their antiplatelet and LDL-lowering effects. In this review, we summarize the currently available evidence on platelet hyperreactivity in PH, the effects of PCSK9 inhibitors on platelets, and their synergism with other drugs used in PH therapy.

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Bi, Ying, Jixiang Chen, Feng Hu, Jing Liu, Man Li, and Lei Zhao. "M2 Macrophages as a Potential Target for Antiatherosclerosis Treatment." Neural Plasticity 2019 (February 21, 2019): 1–21. http://dx.doi.org/10.1155/2019/6724903.

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Atherosclerosis is a chronic progressive inflammation course, which could induce life-threatening diseases such as stroke and myocardial infarction. Optimal medical treatments for atherosclerotic risk factors with current antihypertensive and lipid-lowering drugs (for example, statins) are widely used in clinical practice. However, many patients with established disease still continue to have recurrent cardiovascular events in spite of treatment with a state-of-the-art therapy. Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of mortality worldwide. Hence, current treatment of atherosclerosis is still far from being satisfactory. Recently, M2 macrophages have been found associated with atherosclerosis regression. The M2 phenotype can secrete anti-inflammatory factors such as IL-10 and TGF-β, promote tissue remodeling and repairing through collagen formation, and clear dying cells and debris by efferocytosis. Therefore, modulators targeting macrophages’ polarization to the M2 phenotype could be another promising treatment strategy for atherosclerosis. Two main signaling pathways, the Akt/mTORC/LXR pathway and the JAK/STAT6 pathway, are found playing important roles in M2 polarization. In addition, researchers have reported several potential approaches to modulate M2 polarization. Inhibiting or activating some kinds of enzymes, affecting transcription factors, or acting on several membrane receptors could regulate the polarization of the M2 phenotype. Besides, biomolecules, for example vitamin D, were found to affect the process of M2 polarization. Pomegranate juice could promote M2 polarization via unclear mechanism. In this review, we will discuss how M2 macrophages affect atherosclerosis regression, signal transduction in M2 polarization, and outline potential targets and compounds that affect M2 polarization, thus controlling the progress of atherosclerosis.

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Kisiel, Bartłomiej, Robert Kruszewski, Aleksandra Juszkiewicz, Anna Raczkiewicz, Artur Bachta, Małgorzata Tłustochowicz, Jadwiga Staniszewska-Varga, et al. "Methotrexate, Cyclosporine A, and Biologics Protect against Atherosclerosis in Rheumatoid Arthritis." Journal of Immunology Research 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/759610.

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Introduction. The risk of cardiovascular disease is increased in rheumatoid arthritis (RA). A meta-analysis showed increased intima media thickness (IMT) in RA. It has been shown that disease modifying antirheumatic drugs (DMARDs) may influence the progression of atherosclerosis. However, it was suggested that biologics may be more efficient than other DMARDs (including methotrexate—MTX) in protecting against atherosclerosis.Objectives. The aim of this study was to assess the influence of different RA characteristics and treatment regimens on IMT and atherosclerotic plaques.Patients and Methods. 317 RA patients and 111 controls were included in the study. IMT was measured in carotid (CIMT) and femoral (FIMT) arteries. Arteries were screened for the presence of plaques.Results. CIMT, FIMT, and prevalence of plaques were lower in patients treated with methotrexate (MTX) ≥ 20 mg/wk, cyclosporine (CsA), or biologics than in patients treated with lower doses of MTX and other disease modifying antirheumatic drugs. No differences in IMT between patients treated with MTX ≥ 20 mg/wk, biologics, or CsA were found.Conclusions. We found a beneficial effect of MTX ≥ 20 mg/wk, biologics, and CsA on atherosclerosis. We do not confirm a stronger influence of biologics on IMT compared with therapeutic doses of MTX.

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Orekhov, Alexander N., Andrey V. Grechko, Elena B. Romanenko, Dongwei Zhang, and Dimitry A. Chistiakov. "Novel Approaches to Anti-atherosclerotic Therapy: Cell-based Models and Herbal Preparations (Review of Our Own Data)." Current Drug Discovery Technologies 17, no. 3 (July 15, 2020): 278–85. http://dx.doi.org/10.2174/1570163816666190101112241.

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Atherosclerosis is a chronic arterial disease characterized by vascular inflammation, accumulation of lipids in the arterial wall, and formation and growth of atherosclerotic plaques followed by ischemia. In subclinical atherosclerosis, cholesterol retention in subendothelial cells leads to induction of local inflammation, generation of foam cells and lesion formation, followed by a chain of other pathogenic events. Atherosclerotic progression can frequently be fatal, since plaque rupture may lead to thrombosis and acute events, such as myocardial infarction, stroke and sudden death. Traditional anti-atherosclerotic therapy is mainly focused on improving the blood lipid profile and does not target various stages of plaque progression. Obviously, treating the disease at initial stages is better than beginning treatment at advanced stages and, in that regard, current atherosclerosis management can be improved. Cholesterol retention is an important component of atherogenesis that precedes plaque formation. Therapeutic targeting of cholesterol retention may be beneficial for preventing further atherogenic progression. For this purpose, we suggest using herbal preparations due to good tolerability and suitability for long-lasting treatment. We developed test systems based on cultured human intimal aortic cells for rapid screening of potential anti-atherogenic drugs. With the help of these test systems, we selected several natural substances with significant anti-atherogenic activity and further use these compounds to prepare herbal preparations for anti-atherosclerotic therapy. These preparations were clinically tested and showed good safety and a potent anti-atherogenic potential.

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Ketelhuth, Daniel F. J., Esther Lutgens, Magnus Bäck, Christoph J. Binder, Jan Van den Bossche, Carolin Daniel, Ingrid E. Dumitriu, et al. "Immunometabolism and atherosclerosis: perspectives and clinical significance: a position paper from the Working Group on Atherosclerosis and Vascular Biology of the European Society of Cardiology." Cardiovascular Research 115, no. 9 (June 22, 2019): 1385–92. http://dx.doi.org/10.1093/cvr/cvz166.

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Abstract Inflammation is an important driver of atherosclerosis, and the favourable outcomes of the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) trial revealed the large potential of anti-inflammatory drugs for the treatment of cardiovascular disease, especially in patients with a pro-inflammatory constitution. However, the complex immune reactions driving inflammation in the vascular wall in response to an atherosclerotic microenvironment are still being unravelled. Novel insights into the cellular processes driving immunity and inflammation revealed that alterations in intracellular metabolic pathways are strong drivers of survival, growth, and function of immune cells. Therefore, this position paper presents a brief overview of the recent developments in the immunometabolism field, focusing on its role in atherosclerosis. We will also highlight the potential impact of immunometabolic markers and targets in clinical cardiovascular medicine.

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HIROSUMI, Jiro, Chie NAKAJIMA, Atsushi NOMOTO, Yoshitaka OHKUSO, Isamu YAMAGUCHI, and Hatsuo AOKI. "Preparation of Atherosclerotic Model by the Cuff Method and Effects of Drugs on the Atherosclerosis." Journal of Japan Atherosclerosis Society 13, no. 6 (1986): 1487–91. http://dx.doi.org/10.5551/jat1973.13.6_1487.

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Jankowski, Piotr, Michel E. Safar, and Kalina Kawecka-Jaszcz. "How Drugs Influencing Central Blood Pressure Prevent Atherosclerosis Complications?" Current Pharmaceutical Biotechnology 13, no. 13 (December 11, 2012): 2449–55. http://dx.doi.org/10.2174/1389201011208062449.

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Jankowski, Piotr, Michel E. Safar, and Kalina Kawecka-Jaszcz. "How Drugs Influencing Central Blood Pressure Prevent Atherosclerosis Complications?" Current Pharmaceutical Biotechnology 13, no. 13 (October 1, 2012): 2449–55. http://dx.doi.org/10.2174/138920112804583078.

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Paoletti, R. "2.C.6 New strategies for drugs in atherosclerosis." Atherosclerosis 134, no. 1-2 (October 1997): 103–4. http://dx.doi.org/10.1016/s0021-9150(97)88589-9.

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Wang, Jintao, and Daniel T. Eitzman. "Do Selective Serotonin Reuptake Inhibitor Antidepressant Drugs Promote Atherosclerosis?" Arteriosclerosis, Thrombosis, and Vascular Biology 38, no. 5 (May 2018): 978–79. http://dx.doi.org/10.1161/atvbaha.118.311052.

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Chobanian, Aram V. "Can Antihypertensive Drugs Reduce Atherosclerosis and Its Clinical Complications." American Journal of Hypertension 7, no. 10_Pt_2 (October 1994): 119S—125S. http://dx.doi.org/10.1093/ajh/7.10.119s.

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Alexander, L., and C. Ballantyne. "Two Drugs Have Potential to Slow Progression of Atherosclerosis." MD Conference Express 8, no. 2 (May 1, 2008): 16–17. http://dx.doi.org/10.1177/155989770800800214.

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Konrad, Ildiko, Susanne Sauer, Lena Orschiedt, Maria Koellnberger, Reinhard Lorenz, Ulrich Walter, Steffen Massberg, and Christian Schulz. "Effect of chronic treatment with acetylsalicylic acid and clopidogrel on atheroprogression and atherothrombosis in ApoE-deficient mice in vivo." Thrombosis and Haemostasis 99, no. 01 (2008): 190–95. http://dx.doi.org/10.1160/th07-03-0235.

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SummaryAcetylsalicylic acid (ASA) and the thienopyridine clopidogrel are established anti-platelet drugs that significantly reduce secondary cardiovascular events in patients with manifest atherosclerosis. However, their impact on atherosclerotic lesion development remains controversial. Four-week-old ApoE-deficient mice were randomly assigned to four groups receiving a cholesterol diet together with either ASA (5 mg/kg), or clopidogrel (25 mg/kg), or a combination of both ASA and clopidogrel, or vehicle for 8–12 weeks. Using intravital microscopy we found that daily administration of ASA in combination with clopidogrel reduces platelet thrombus formation following rupture of atherosclerotic plaque in vivo by ∼50%. However, therapy with ASA or clopidogrel alone, or in combination for a period of 8–12 weeks had no significant effect on adhesion of platelets to dysfunctional endothelial cells or on atherosclerotic lesion formation in the aortic root or the carotid artery. In conclusion, anti-platelet therapy is effective in reducing platelet adhesion and subsequent thrombus formation following rupture of atherosclerotic plaque in vivo. However, our data do not support a role of either drug in the primary prevention of atherosclerosis in ApoE-deficient mice.

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Zhang, Yuchao, Gang Xu, Maozhen Chen, Ziliang Chen, Mingyang Shen, and Ping Wang. "Application of Hydrogen Peroxide Sensitive Fluorescen Nanoparticles in Atherosclerosis." Journal of Nanoscience and Nanotechnology 21, no. 2 (February 1, 2021): 833–42. http://dx.doi.org/10.1166/jnn.2021.18670.

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ROS plays an important role in the formation of atherosclerotic plaque, especially hydrogen peroxide, which can stimulate macrophages to express pro-inflammatory cytokines and chemokines to enhance the inflammatory activity of macrophages. Therefore, the development of drugs with sensitive release of hydrogen peroxide is safe and effective for the treatment of atherosclerosis The side chain hydroxyl groups of pHEMA were grafted with oxalylsimvastatin (SIM), fluoropolyethylene glycol (fpeg) and macrophage target molecule ISO-1 to prepare hydrogen peroxide sensitive fluorescent drug loaded nanomicelles (phema-simfpeg-iso-1). By using hydrogen peroxide sensitive and controlled-release drug, it can target macrophage, at the same time, improve the characteristics of traditional polyethylene glycol only as hydrophilic chain, and synthesize polyethylene glycol with fluorescence function, so that the polymer can have probe ability without modifying fluorescence substance, which is suitable for the diagnosis and treatment of atherosclerosis. The results show that the water-soluble nanoparticles show good biocompatibility and peroxide Hydrogen sensitivity and fluorescence ability provide new materials for the development of a nano system for the diagnosis and treatment of atherosclerosis.

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Pinkaew, Decha, Rachel J. Le, Yanjie Chen, Mahmoud Eltorky, Ba-Bie Teng, and Ken Fujise. "Fortilin reduces apoptosis in macrophages and promotes atherosclerosis." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 10 (November 15, 2013): H1519—H1529. http://dx.doi.org/10.1152/ajpheart.00570.2013.

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Atherosclerosis, a deadly disease insufficiently addressed by cholesterol-lowering drugs, needs new therapeutic strategies. Fortilin, a 172-amino acid multifunctional polypeptide, binds p53 and blocks its transcriptional activation of Bax, thereby exerting potent antiapoptotic activity. Although fortilin-overexpressing mice reportedly exhibit hypertension and accelerated atherosclerosis, it remains unknown if fortilin, not hypertension, facilitates atherosclerosis. Our objective was to test the hypothesis that fortilin in and of itself facilitates atherosclerosis by protecting macrophages against apoptosis. We generated fortilin-deficient ( fortilin+/−) mice and wild-type counterparts ( fortilin+/+) on a LDL receptor ( Ldlr)−/− apolipoprotein B mRNA editing enzyme, catalytic polypeptide 1 ( Apobec1)−/− hypercholesterolemic genetic background, incubated them for 10 mo on a normal chow diet, and assessed the degree and extent of atherosclerosis. Despite similar blood pressure and lipid profiles, fortilin+/− mice exhibited significantly less atherosclerosis in their aortae than their fortilin +/+ littermate controls. Quantitative immunostaining and flow cytometry analyses showed that the atherosclerotic lesions of fortilin+/− mice contained fewer macrophages than those of fortilin+/+ mice. In addition, there were more apoptotic cells in the intima of fortilin+/− mice than in the intima of fortilin+/+ mice. Furthermore, peritoneal macrophages from fortilin+/− mice expressed more Bax and underwent increased apoptosis, both at the baseline level and in response to oxidized LDL. Finally, hypercholesterolemic sera from Ldlr−/− Apobec1−/− mice induced fortilin in peritoneal macrophages more robustly than sera from control mice. In conclusion, fortilin, induced in the proatherosclerotic microenvironment in macrophages, protects macrophages against Bax-induced apoptosis, allows them to propagate, and accelerates atherosclerosis. Anti-fortilin therapy thus may represent a promising next generation antiatherosclerotic therapeutic strategy.

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Summerhill, Grechko, Yet, Sobenin, and Orekhov. "The Atherogenic Role of Circulating Modified Lipids in Atherosclerosis." International Journal of Molecular Sciences 20, no. 14 (July 20, 2019): 3561. http://dx.doi.org/10.3390/ijms20143561.

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Lipid accumulation in the arterial wall is a crucial event in the development of atherosclerotic lesions. Circulating low-density lipoprotein (LDL) is the major source of lipids that accumulate in the atherosclerotic plaques. It was discovered that not all LDL is atherogenic. In the blood plasma of atherosclerotic patients, LDL particles are the subject of multiple enzymatic and non-enzymatic modifications that determine their atherogenicity. Desialylation is the primary and the most important atherogenic LDL modification followed by a cascade of other modifications that also increase blood atherogenicity. The enzyme trans-sialidase is responsible for the desialylation of LDL, therefore, its activity plays an important role in atherosclerosis development. Moreover, circulating modified LDL is associated with immune complexes that also have a strong atherogenic potential. Moreover, it was shown that antibodies to modified LDL are also atherogenic. The properties of modified LDL were described, and the strong evidence indicating that it is capable of inducing intracellular accumulation of lipids was presented. The accumulated evidence indicated that the molecular properties of modified LDL, including LDL-containing immune complexes can serve as the prognostic/diagnostic biomarkers and molecular targets for the development of anti-atherosclerotic drugs.

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Yanai, Hidekatsu, and Hiroshi Yoshida. "Beneficial Effects of Adiponectin on Glucose and Lipid Metabolism and Atherosclerotic Progression: Mechanisms and Perspectives." International Journal of Molecular Sciences 20, no. 5 (March 8, 2019): 1190. http://dx.doi.org/10.3390/ijms20051190.

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Circulating adiponectin concentrations are reduced in obese individuals, and this reduction has been proposed to have a crucial role in the pathogenesis of atherosclerosis and cardiovascular diseases associated with obesity and the metabolic syndrome. We focus on the effects of adiponectin on glucose and lipid metabolism and on the molecular anti-atherosclerotic properties of adiponectin and also discuss the factors that increase the circulating levels of adiponectin. Adiponectin reduces inflammatory cytokines and oxidative stress, which leads to an improvement of insulin resistance. Adiponectin-induced improvement of insulin resistance and adiponectin itself reduce hepatic glucose production and increase the utilization of glucose and fatty acids by skeletal muscles, lowering blood glucose levels. Adiponectin has also β cell protective effects and may prevent the development of diabetes. Adiponectin concentration has been found to be correlated with lipoprotein metabolism; especially, it is associated with the metabolism of high-density lipoprotein (HDL) and triglyceride (TG). Adiponectin appears to increase HDL and decrease TG. Adiponectin increases ATP-binding cassette transporter A1 and lipoprotein lipase (LPL) and decreases hepatic lipase, which may elevate HDL. Increased LPL mass/activity and very low density lipoprotein (VLDL) receptor and reduced apo-CIII may increase VLDL catabolism and result in the reduction of serum TG. Further, adiponectin has various molecular anti-atherosclerotic properties, such as reduction of scavenger receptors in macrophages and increase of cholesterol efflux. These findings suggest that high levels of circulating adiponectin can protect against atherosclerosis. Weight loss, exercise, nutritional factors, anti-diabetic drugs, lipid-lowering drugs, and anti-hypertensive drugs have been associated with an increase of serum adiponectin level.

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Journal articles on the topic 'Atherosclerosis Drugs'

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