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Journal articles on the topic 'Atherosclerosis: pathology'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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1

Woolf, N. "Pathology of atherosclerosis." British Medical Bulletin 46, no. 4 (1990): 960–85. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072448.

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2

Donosepoetro, Marsetio. "MOLECULAR PATHOLOGY OF CEREBROVASCULAR ATHEROSCLEROSIS." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 12, no. 1 (2018): 16. http://dx.doi.org/10.24293/ijcpml.v12i1.835.

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Cerebrovascular disease are the third most common cause of death in Western countries. The most frequent manifestation of disease is a sudden episode of neurological deficit termed stroke which is the result of cerebral haemorrhage or cerebral infaction in the mayority of cases. Stroke secondary to atherosclerosis is most common in people over 50 years old.The incidence of stroke rises dramatically with ages, with the risk doubling with each decade after 35 years old. About 5 % of people over 65 years old have at least one stroke. Atherosclerosis is condition where fatty acid deposits occur in

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3

Watson, Shana R., and Susan M. Lessner. "(Second) Harmonic Disharmony: Nonlinear Microscopy Shines New Light on the Pathology of Atherosclerosis." Microscopy and Microanalysis 22, no. 3 (2016): 589–98. http://dx.doi.org/10.1017/s1431927616000842.

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AbstractThere has been increasing interest in second harmonic generation (SHG) imaging approaches for the investigation of atherosclerosis due to the deep penetration and three-dimensional sectioning capabilities of the nonlinear optical microscope. Atherosclerosis involves remodeling or alteration of the collagenous framework in affected vessels. The disease is often characterized by excessive collagen deposition and altered collagen organization. SHG has the capability to accurately characterize collagen structure, which is an essential component in understanding atherosclerotic lesion devel

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4

TAKANO, Tatsuya, and Hiroko TAKAHASHI. "Atherosclerosis from Molecular Pathology." Journal of Japan Atherosclerosis Society 17, no. 3 (1989): 407–12. http://dx.doi.org/10.5551/jat1973.17.3_407.

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5

Rainger, G. Ed, and Gerard B. Nash. "Cellular Pathology of Atherosclerosis." Circulation Research 88, no. 6 (2001): 615–22. http://dx.doi.org/10.1161/01.res.88.6.615.

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6

Wang, Tao, Daniel Palucci, Kelsey Law, Bobby Yanagawa, Jennifer Yam, and Jagdish Butany. "Atherosclerosis: pathogenesis and pathology." Diagnostic Histopathology 18, no. 11 (2012): 461–67. http://dx.doi.org/10.1016/j.mpdhp.2012.09.004.

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7

Tull, Samantha P., Steve I. Anderson, Sascha C. Hughan, Steve P. Watson, Gerard B. Nash, and G. Ed Rainger. "Cellular Pathology of Atherosclerosis." Circulation Research 98, no. 1 (2006): 98–104. http://dx.doi.org/10.1161/01.res.0000198386.69355.87.

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8

Maiuri, Maria Chiara, Gianluca Grassia, Andrew M. Platt, Rosa Carnuccio, Armando Ialenti, and Pasquale Maffia. "Macrophage Autophagy in Atherosclerosis." Mediators of Inflammation 2013 (2013): 1–14. http://dx.doi.org/10.1155/2013/584715.

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Macrophages play crucial roles in atherosclerotic immune responses. Recent investigation into macrophage autophagy (AP) in atherosclerosis has demonstrated a novel pathway through which these cells contribute to vascular inflammation. AP is a cellular catabolic process involving the delivery of cytoplasmic contents to the lysosomal machinery for ultimate degradation and recycling. Basal levels of macrophage AP play an essential role in atheroprotection during early atherosclerosis. However, AP becomes dysfunctional in the more advanced stages of the pathology and its deficiency promotes vascul

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9

Kolodgie, Frank D., Gaku Nakazawa, Giuseppe Sangiorgi, Elena Ladich, Allen P. Burke, and Renu Virmani. "Pathology of Atherosclerosis and Stenting." Neuroimaging Clinics of North America 17, no. 3 (2007): 285–301. http://dx.doi.org/10.1016/j.nic.2007.03.006.

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10

Kozhanova, T. V., E. V. Neudakhin, S. S. Zhilina, et al. "THE GENETIC SUSCEPTIBILITY TO ATHEROSCLEROSIS." Russian Archives of Internal Medicine 8, no. 6 (2018): 407–17. http://dx.doi.org/10.20514/2226-67042018-8-6-407-417.

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Atherosclerosis is a complex multifocal arterial disease involving interactions of multiple genetic and environmental factors. Atherosclerosis is the main cause of death and disability in developed countries, while in developing countries the incidence of this pathology is growing rapidly. Advances in techniques of molecular genetics have revealed that genetic polymorphisms significantly influence susceptibility to atherosclerotic vascular diseases. A large number of candidate genes, genetic polymorphisms and susceptibility loci associated with atherosclerotic diseases have been identified in

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11

Dolzhenko, A., T. Richter, and S. Sagalovsky. "ROLE OF NUCLEAR FACTOR (NF)-kB PROTEIN IN ATHEROSCLEROSIS AND DIABETES: A POTENTIAL THERAPEUTIC TARGET." Problems of Endocrine Pathology 54, no. 4 (2015): 87–104. http://dx.doi.org/10.21856/j-pep.2015.4.11.

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Cardiovascular diseases and diabetes are the leading cause of morbidity and mortality in all countries. Atherosclerosis, the background for many cardiovascular diseases, is characterized by the accumulation of lipid and fibrotic entities in large arteries and bears many similarities with chronic inflammatory diseases such as diabetes. Common features include extravasation of blood-derived leukocytes, as well as production of cytokines, chemokines and matrix-degrading enzymes. There are also many shared signaling pathways, including activation of the nuclear factor kB (NF-kB) cascade. In the pa

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12

Otsuka, Fumiyuki, Satoshi Yasuda, Teruo Noguchi, and Hatsue Ishibashi-Ueda. "Pathology of coronary atherosclerosis and thrombosis." Cardiovascular Diagnosis and Therapy 6, no. 4 (2016): 396–408. http://dx.doi.org/10.21037/cdt.2016.06.01.

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13

Simonetti, L., R. Agati, and M. Leonardi. "Carotid Atherosclerosis from Pathology to Neuroradiology." Rivista di Neuroradiologia 16, no. 1 (2003): 15–26. http://dx.doi.org/10.1177/197140090301600102.

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We describe the correlations between the pathological anatomy of atheromatous plaque and neuroradiological findings, discussing the morphological features of plaque surface and location, the histopathological and structural characteristics of the plaque and why intramural haemorrhage occurs.

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14

Foks, Amanda C., and Ilze Bot. "Preface: Pathology and Pharmacology of Atherosclerosis." European Journal of Pharmacology 816 (December 2017): 1–2. http://dx.doi.org/10.1016/j.ejphar.2017.10.052.

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15

Nettersheim, Felix Sebastian, Lauren De Vore, and Holger Winkels. "Vaccination in Atherosclerosis." Cells 9, no. 12 (2020): 2560. http://dx.doi.org/10.3390/cells9122560.

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Atherosclerosis is the major underlying pathology of cardiovascular diseases that together are the leading cause of death worldwide. The formation of atherosclerotic plaques is driven by chronic vascular inflammation. Although several risk factors have been identified and significant progress in disease prevention and treatment has been made, no therapeutic agents targeting inflammation are clinically available. Recent clinical trials established the potential of anti-inflammatory therapies as a treatment of atherosclerosis. However, adverse impacts on host defense have raised safety concerns

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16

Alonso-Piñeiro, Jose Angel, Almudena Gonzalez-Rovira, Ismael Sánchez-Gomar, Juan Antonio Moreno, and Ma Carmen Durán-Ruiz. "Nrf2 and Heme Oxygenase-1 Involvement in Atherosclerosis Related Oxidative Stress." Antioxidants 10, no. 9 (2021): 1463. http://dx.doi.org/10.3390/antiox10091463.

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Atherosclerosis remains the underlying process responsible for cardiovascular diseases and the high mortality rates associated. This chronic inflammatory disease progresses with the formation of occlusive atherosclerotic plaques over the inner walls of vascular vessels, with oxidative stress being an important element of this pathology. Oxidation of low-density lipoproteins (ox-LDL) induces endothelial dysfunction, foam cell activation, and inflammatory response, resulting in the formation of fatty streaks in the atherosclerotic wall. With this in mind, different approaches aim to reduce oxida

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17

Blumenthal, Herman T. "Atherosclerosis." Human Pathology 16, no. 9 (1985): 966. http://dx.doi.org/10.1016/s0046-8177(85)80142-8.

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18

Ambade, Vipul Namdeorao, Hemant Vasant Godbole, and Anil Krishnaram Batra. "Atherosclerosis." American Journal of Forensic Medicine and Pathology 29, no. 3 (2008): 279–80. http://dx.doi.org/10.1097/paf.0b013e31817e792b.

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19

Natarajan, Rama, and Qiangjun Cai. "Monocyte retention in the pathology of atherosclerosis." Future Cardiology 1, no. 3 (2005): 331–40. http://dx.doi.org/10.1517/14796678.1.3.331.

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20

Badimon, Lina. "Atherosclerosis and Thrombosis: Lessons from Animal Models." Thrombosis and Haemostasis 86, no. 07 (2001): 356–65. http://dx.doi.org/10.1055/s-0037-1616233.

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SummaryAtherothrombosis defines the occurrence of thrombosis on athero-sclerotic lesions. Atherosclerosis is the most prevalent disease of our time and its thrombotic complications are responsible for an exceedingly high number of deaths and disabilities. Over the past few years, experimental investigation and clinical and pathologic observations have led to a better understanding of how a thrombus forms and also of its incidence in acute ischemic syndromes. A thrombus is usually found secondary to atherosclerotic plaque disruption. Mural thrombosis, also at the site of plaque rupture, is an i

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21

Poznyak, Anastasia V., Alexandra A. Melnichenko, Reinhard Wetzker, Elena V. Gerasimova, and Alexander N. Orekhov. "NLPR3 Inflammasomes and Their Significance for Atherosclerosis." Biomedicines 8, no. 7 (2020): 205. http://dx.doi.org/10.3390/biomedicines8070205.

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Atherosclerosis is a serious disorder, with numerous potential complications such as cardiovascular disease, ischemic stroke, and myocardial infarction. The origin of atherosclerosis is related to chronic inflammation, lipid metabolism alterations, and oxidative stress. Inflammasomes are the cytoplasmic multiprotein complex triggering the activation of inflammatory response. NLRP3 inflammasomes have a specific activation pathway that involves numerous stimuli, including a wide range of PAMPs and DAMPs. Recent studies of atherosclerotic pathology are focused on the mitochondria that appear to b

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22

Smedlund, Kathryn, Prabhatachandra Dube, and Guillermo Vazquez. "Early steatohepatitis in hyperlipidemic mice with endothelial-specific gain of TRPC3 function precedes changes in aortic atherosclerosis." Physiological Genomics 48, no. 8 (2016): 644–49. http://dx.doi.org/10.1152/physiolgenomics.00067.2016.

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Nonalcoholic fatty liver disease (NAFLD) and its more advanced form nonalcoholic steatohepatitis (NASH) are the most common chronic liver diseases in developed countries. Moreover, NAFLD and NASH are considerable risk factors for atherosclerosis, the most frequent vascular pathology in these and other metabolic diseases. Despite this strong connection, current knowledge of the relationship between NAFLD/NASH and atherosclerosis is scarce. Recently, we studied hyperlipidemic Apoe knockout mice with endothelial-specific gain of transient receptor potential canonical 3 channel function (TgESTRPC3

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23

Evsikov, E. M., V. I. Vechorko, N. V. Teplova, M. H. Zhapueva, and N. G. Artamonova. "Factors and mechanisms of arterial hypertension development in patients with atherosclerosis of lower limb arteries." Cardiovascular Therapy and Prevention 18, no. 1 (2019): 150–55. http://dx.doi.org/10.15829/1728-8800-2019-1-150-155.

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The article contains information about the frequency of development of arterial hypertension (AH), the features and causes of its development in patients with peripheral atherosclerosis. AH in patients with chronic atherosclerotic diseases of lower limb arteries and acute thrombotic occlusion complicates the course of this pathology. In most patients, the opinion that AH associated with atherosclerosis due to affection of renal arteries is generally accepted. Currently, an important practical question remains about the possible negative impact of intensive antihypertensive therapy with a signi

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24

St. Paul, Amanda, Cali B. Corbett, Rachael Okune, and Michael V. Autieri. "Angiotensin II, Hypercholesterolemia, and Vascular Smooth Muscle Cells: A Perfect Trio for Vascular Pathology." International Journal of Molecular Sciences 21, no. 12 (2020): 4525. http://dx.doi.org/10.3390/ijms21124525.

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Cardiovascular disease is the leading cause of morbidity and mortality in the Western and developing world, and the incidence of cardiovascular disease is increasing with the longer lifespan afforded by our modern lifestyle. Vascular diseases including coronary heart disease, high blood pressure, and stroke comprise the majority of cardiovascular diseases, and therefore represent a significant medical and socioeconomic burden on our society. It may not be surprising that these conditions overlap and potentiate each other when we consider the many cellular and molecular similarities between the

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25

Shaw, Daniel James, Rachel Seese, Sreenivasan Ponnambalam, and Ramzi Ajjan. "The role of lectin-like oxidised low-density lipoprotein receptor-1 in vascular pathology." Diabetes and Vascular Disease Research 11, no. 6 (2014): 410–18. http://dx.doi.org/10.1177/1479164114547704.

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The lectin-like oxidised low-density lipoprotein receptor-1 (LOX-1) is a vascular scavenger receptor that plays a central role in the pathogenesis of atherothrombotic disease, which remains the main cause of mortality in the Western population. Recent evidence indicates that targeting LOX-1 represents a credible strategy for the management vascular disease and the current review explores the role of this molecule in the diagnosis and treatment of atherosclerosis. LOX-1-mediated pro-atherogenic effects can be inhibited by anti-LOX-1 monoclonal antibodies and procyanidins, whereas downregulation

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26

Mazurov, V. I., S. V. Stolov, I. B. Belyaeva, and E. A. Trofimov. "THE PARTICIPATION OF IMMUNE AND INFLAMMATORY MECHANISMSIN THE PATHOGENESIS OF CORONARY ATHEROSCLEROSIS." HERALD of North-Western State Medical University named after I.I. Mechnikov 7, no. 4 (2015): 13–23. http://dx.doi.org/10.17816/mechnikov20157413-23.

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It was revealed that in development of a coronary atherosclerosis, participate the immune-mediated mechanisms. In blood of patients with coronary atherosclerosis the maintenance of the basic classes cytokines (IL-1 β, IL-2, IL-6, IL-8, TNF-a) were increased. Development of acute coronary insufficiency is accompanied by additional increase of levels of the data cytokines. The accessory of the cytokine activity to a coronary atherosclerosis was confirmed at studying the maintenance mRNA cytokines in a vascular wall. Thus in a zone atheromatous (aorta) it was synthesized mainly mRNA IL-2, while i

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27

Kohler, Ted R. "Atherosclerosis: Pathology of the Vasculature in Live Patients." Annals of Vascular Surgery 14, no. 3 (2000): 308–9. http://dx.doi.org/10.1007/s100169910057.

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28

WACHTER, KERRI. "Lewy Body Pathology Tied to Cerebral Atherosclerosis Severity." Clinical Neurology News 3, no. 12 (2007): 10. http://dx.doi.org/10.1016/s1553-3212(08)70012-8.

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29

Matsumura, Jon. "Atherosclerosis: pathology of the vasculature in live patients." Journal of Vascular Surgery 31, no. 3 (2000): 630. http://dx.doi.org/10.1067/mva.2000.104481.

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30

Davies, M. J. "Pathology of atherosclerosis, plaque disruption, and thrombus formation." Current Opinion in Cardiology 4, no. 4 (1989): 464–67. http://dx.doi.org/10.1097/00001573-198908000-00002.

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31

STEWARTPHILLIPS, J., and J. LOUGH. "Pathology of atherosclerosis in cholesterol-fed, susceptible mice." Atherosclerosis 90, no. 2-3 (1991): 211–18. http://dx.doi.org/10.1016/0021-9150(91)90117-l.

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32

Chejfec, Gregorio. "Atherosclerosis: Pathology of the Vasculature in Live Patients." Archives of Pathology & Laboratory Medicine 124, no. 9 (2000): 1386. http://dx.doi.org/10.5858/2000-124-1386a-apotvi.

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33

Mirzarakhmetova, Dilbar T., and Yulduz Yusupbaevna Baltaeva. "Molecular Genetic Analysis Of C-X-C Motif Chemokine Ligand 9 (CXCL9) As A Novel Biomarker In Atherosclerosis." American Journal of Applied sciences 3, no. 05 (2021): 24–30. http://dx.doi.org/10.37547/tajas/volume03issue05-05.

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For almost a century, many have considered lipids as the sine qua non of atherosclerosis. However, in 1856 Rudolf Virchow introduced a theory that inflammation is the driving force of atherogenesis. Recruitment of blood leukocytes to the injured vascular endothelium characterizes the initiation and progression of atherosclerosis and involves many inflammatory mediators, modulated by cells of both innate and adaptive immunity. The pro-inflammatory cytokine, interferon (IFN)-γ derived from T cells, is vital for both innate and adaptive immunity and is also expressed at high levels in atheroscler

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34

Glushkov, Nikolay I., Michael A. Ivanov, Petr D. Puzdryak, Kristina V. Samko, Alina A. Isakova, and Anastasia S. Artemova. "Metabolic disorder and outcomes of reconstructive interventions in patients with peripheral arterial disease." HERALD of North-Western State Medical University named after I.I. Mechnikov 11, no. 3 (2019): 33–40. http://dx.doi.org/10.17816/mechnikov201911333-40.

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The purpose of this study was to assess the effect of metabolic disorders on the effects of revascularization in patients with obliterating atherosclerosis. Materials and methods. The reconstruction was performed in 253 patients with femoral-tibial arterial segment lesion (98 open operations, 116 endovascular interventions and 39 patients were treated with hybrid technique). Results. Endovascular revascularization techniques are justified in case of disorders of carbohydrate metabolism. Conventional operations remain the method of choice in the case of those variants of atheroscler

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35

Zernecke, Alma. "MicroRNAs in the regulation of immune cell functions – implications for atherosclerotic vascular disease." Thrombosis and Haemostasis 107, no. 04 (2012): 626–33. http://dx.doi.org/10.1160/th11-08-0603.

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SummaryRegarded as a chronic inflammatory disease of the vessel wall, the development of atherosclerotic lesions is shaped by immune responses and their regulation. Macrophages and dendritic cells are positioned at the crossroad of innate and adaptive immune responses by sensing atherogenic danger signals and by taking up and presenting antigens. T helper cells and auto-antibodies produced by B cells, together with their cytokine responses in turn modulate atheroprogression. In addition, platelets contribute to atherosclerosis by multiple pathways. microRNAs (miRNAs) that post-transcriptionall

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36

Gheorghita, Dorottya, Gabriella Eördegh, Ferenc Nagy, and Márk Antal. "A fogágybetegség mint az atheroscleroticus cardiovascularis betegség rizikófaktora." Orvosi Hetilap 160, no. 11 (2019): 419–25. http://dx.doi.org/10.1556/650.2019.31301.

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Abstract: Cardiovascular disease is recognized as the leading cause of death and disability in the world. The majority of these deaths can be attributed to atherosclerotic disease and thromboembolic events leading to ischemic heart disease and stroke. The role of inflammation is well recognized in the pathogenesis of atherosclerosis and atherothrombosis. Increasing number of studies support the hypothesis that periodontal disease, specifically periodontitis, is a potential risk factor for atherosclerosis and thus cardiovascular disease. Chronic infections of periodontal pockets act as reservoi

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37

Zhou, Cheng-Hua, Lan-Lan Liu, Yu-Qing Wu, Zheng Song та Shu-Hua Xing. "Enhanced expression of salusin-β contributes to progression of atherosclerosis in LDL receptor deficient mice". Canadian Journal of Physiology and Pharmacology 90, № 4 (2012): 463–71. http://dx.doi.org/10.1139/y2012-022.

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Atherosclerosis is an important underlying pathology of cardiovascular diseases. The aim of this study was to observe the expression of salusin-β, a new vasoactive peptide, in vascular tissues of low-density lipoprotein receptor deficient (LDLR–/–) mice, and to evaluate the effect of salusin-β on the development of atherosclerosis in LDLR–/– mice. Six-week-old, male LDLR–/– mice were subcutaneously injected with salusin-β or the vehicle, once a day for 12 weeks. The expressions of salusin-β in both mRNA and peptide levels were determined by reverse transcription – polymerase chain reaction, We

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38

Giménez, Virna M. Martín, Alejandra B. Camargo, Diego Kassuha, and Walter Manucha. "Nanotechnological Strategies as Smart ways for Diagnosis and Treatment of the Atherosclerosis." Current Pharmaceutical Design 24, no. 39 (2019): 4681–84. http://dx.doi.org/10.2174/1381612825666190110154609.

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Atherosclerosis provokes a continuous worsening of affected vessels causing a blood flow diminution with several complications and with clinical manifestations that generally appear in advanced phases of the illness. Hence, the conventional therapies are not enough because the atherosclerotic injuries are often irrevocable. For this reason, emerges the necessity to implement smart ways of drug supply and develop new therapeutic targets that decrease the advance atherosclerotic lesion. It results due to particular interest to use new tools for prevention, diagnosis, and treatment of this cardio

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39

B.M.W. "Prostacyclin and atherosclerosis." Human Pathology 16, no. 3 (1985): 201. http://dx.doi.org/10.1016/s0046-8177(85)80001-0.

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40

Ball, R. Y., and M. J. Mitchinson. "Atherosclerosis: New horizons." Human Pathology 16, no. 11 (1985): 1179–80. http://dx.doi.org/10.1016/s0046-8177(85)80198-2.

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41

Majno, Guido, Isabelle Joris, and Thomas Zand. "Atherosclerosis: New horizons." Human Pathology 16, no. 1 (1985): 3–5. http://dx.doi.org/10.1016/s0046-8177(85)80207-0.

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42

Sinzinger, H., I. Virgolini, A. GazsÓ, and J. O’grady. "Eicosanoids in atherosclerosis." Experimental pathology 43, no. 1-2 (1991): 2–19. http://dx.doi.org/10.1016/s0232-1513(11)80133-7.

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43

Gupta, Rajiv Kumar, Ruchita Tyagi, Vikrampal Singh, et al. "Morphological spectrum of atherosclerotic lesions in a tertiary care Institute in Punjab." Asian Journal of Medical Sciences 10, no. 1 (2018): 19–24. http://dx.doi.org/10.3126/ajms.v10i1.21664.

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Background: The incidence of coronary artery disease (CAD) has risen considerably in developing world due to industrialization, urbanisation and lifestyle changes, especially among Indians and South Asians. The onset of CAD has been seen to occur at an early age and the severity of the disease and mortality associated with CAD has also increased. The pathology of atherosclerosis needs to be re-evaluated to develop targeted therapy which can contain the disease process at the earliest stage. Aims and Objectives: Most of the morphological studies on atherosclerosis have been done on autops

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44

Bergan, John J. "Syndromes of Atherosclerosis: Correlations of Clinical Imaging and Pathology." Chest 113, no. 1 (1998): A—19. http://dx.doi.org/10.1016/s0012-3692(16)39592-7.

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45

Virmani, Renu. "Pathology of Carotid Atherosclerosis in Symptomatic and Asymptomatic Disease." Journal of Vascular and Interventional Radiology 15, no. 2 (2004): P26. http://dx.doi.org/10.1016/s1051-0443(04)70053-6.

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46

Yarchoan, M., S. X. Xie, M. A. Kling, et al. "Cerebrovascular atherosclerosis correlates with Alzheimer pathology in neurodegenerative dementias." Brain 135, no. 12 (2012): 3749–56. http://dx.doi.org/10.1093/brain/aws271.

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47

Podzolkov, V. I., A. E. Pokrovskaya, and O. I. Panasenko. "Vitamin D deficiency and cardiovascular pathology." Terapevticheskii arkhiv 90, no. 9 (2018): 144–50. http://dx.doi.org/10.26442/terarkh2018909144-150.

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Vitamin D deficiency is widespread worldwide and present in about 30-50% of population. In most cases, this problem is associated with musculoskeletal system pathology: rickets in children, and osteomalacia or osteoporosis in adults. However, in recent years, convincing data was obtained on the links between vitamin D deficiency and cardiovascular pathology. Low Vitamin D levels in humans are associated with the unfavorable cardiovascular risk factors, such as arterial hypertension (AH), diabetes mellitus, and dyslipidemia, which are the predictors of the severe cardiovascular diseases, includ

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48

Heine, G. H., and M. Hristov. "Monocyte subsets in atherosclerosis." Hämostaseologie 35, no. 02 (2015): 105–12. http://dx.doi.org/10.5482/hamo-14-08-0030.

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SummaryEndothelial dysfunction and chronic inflammation of the arterial wall continuously drive the development of atherosclerotic lesions. Monocytes, as cells of the innate immunity, are particularly involved in this process. In the last decade, heterogeneity of circulating monocytes has widely been acknowledged, and a recent consensus nomenclature subdivides classical, intermediate and nonclassical monocytes. Accumulating experimental and clinical data suggest a differential, subsetspecific contribution of monocytes to the pathology of atherosclerosis.This review summarizes recent key findin

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49

Kuiper, Johan, and Saskia de Jager. "Vaccination strategies in atherosclerosis." Thrombosis and Haemostasis 106, no. 11 (2011): 796–803. http://dx.doi.org/10.1160/th11-05-0369.

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SummaryThe treatment of atherosclerosis is currently based on lipid lowering in combination with anti-inflammatory therapies that slow the progression of atherosclerosis. Still, we are not able to fully inhibit the formation or progression of atherosclerotic lesions. A very effective strategy in other disease pathologies is vaccination, in which the body is challenged with the culprit protein or micro-organism in order to create a highly specific humoral immune-response. Immunisation can typically be divided into active or passive immunisation. Active immunisation occurs naturally when the bod

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50

Kagawa, Y., K. Hirayama, E. Uchida, et al. "Systemic atherosclerosis in dogs: Histopathological and immunohistochemical studies of atherosclerotic lesions." Journal of Comparative Pathology 118, no. 3 (1998): 195–206. http://dx.doi.org/10.1016/s0021-9975(05)80126-4.

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