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Artykuły w czasopismach na temat „Reverse cholesterol transport pathway”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Kuypers, Frans A., Sandra Larkin, Jenifer Beckstead, Michael Oda, Kazumitsu Ueda, and Robert O. Ryan. "Red Blood Cells Facilitate Reverse Cholesterol Transport." Blood 104, no. 11 (2004): 1589. http://dx.doi.org/10.1182/blood.v104.11.1589.1589.

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Abstract Lecithin:cholesterol acyl transferase (LCAT)-dependent conversion of cholesterol (CH) to cholesteryl ester (CE), a key component of the reverse cholesterol transport (RCT) pathway, is essential for cholesterol processing. We hypothesized that red blood cells (RBCs) function in this pathway by facilitating phosphatidylcholine (PC) re-generation from LCAT-derived lysophosphatidylcholine (LPC). Addition of 14C-oleate to fresh RBCs resulted in an ATP-dependent incorporation of radiolabel into PC via the Lands pathway. Prior depletion of red cell LPC content reduced the incorporation of 14

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Zhang, Xinyuan, Kaiyue Wang, Ling Zhu, and Qiyun Wang. "Reverse Cholesterol Transport Pathway and Cholesterol Efflux in Diabetic Retinopathy." Journal of Diabetes Research 2021 (October 26, 2021): 1–11. http://dx.doi.org/10.1155/2021/8746114.

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Cholesterol esters, synthesized from cholesterol with long-chain fatty acids, are essential components of plasma lipoproteins and cell membranes that participate in various metabolic processes in the body. Cholesterol can be excreted through the cholesterol reverse transport (RCT) pathway when excessive cholesterol is produced in the extrahepatic cells, which is regulated by the liver X receptor (LXR) and its downstream regulators ATP-binding cassette subfamily A member 1 (ABCA1) and ATP-binding cassette subfamily G member 1 (ABCG1) genes. Abnormal cholesterol metabolism is closely associated

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Moradi, Hamid, Jun Yuan, Zhemin Ni, Keith Norris, and Nosratola D. Vaziri. "Reverse Cholesterol Transport Pathway in Experimental Chronic Renal Failure." American Journal of Nephrology 30, no. 2 (2009): 147–54. http://dx.doi.org/10.1159/000210020.

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Wang, David Q. H., Piero Portincasa, and Patrick Tso. "Transintestinal cholesterol excretion: A secondary, nonbiliary pathway contributing to reverse cholesterol transport." Hepatology 66, no. 4 (2017): 1337–40. http://dx.doi.org/10.1002/hep.29341.

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Alam, Khairul, Robert S. Meidell, and David K. Spady. "Effect of Up-regulating Individual Steps in the Reverse Cholesterol Transport Pathway on Reverse Cholesterol Transport in Normolipidemic Mice." Journal of Biological Chemistry 276, no. 19 (2001): 15641–49. http://dx.doi.org/10.1074/jbc.m010230200.

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Bellanger, Natacha, Alexina Orsoni, Zélie Julia, et al. "Atheroprotective Reverse Cholesterol Transport Pathway Is Defective in Familial Hypercholesterolemia." Arteriosclerosis, Thrombosis, and Vascular Biology 31, no. 7 (2011): 1675–81. http://dx.doi.org/10.1161/atvbaha.111.227181.

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Chao, W. T., and V. C. Yang. "Visualization of Uptake of High-Density Lipoprotein by Rat Aortic Endothelial Cells and Smooth Mus.Cle Cells in Vitro." Microscopy and Microanalysis 6, S2 (2000): 482–83. http://dx.doi.org/10.1017/s1431927600034905.

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The high concentration of low-density lipoprotein in the plasma is the major risk factor of atherosclerosis. On the other hand, another plasma lipoprotein—high-density lipoprotein (HDL) — is inversely correlated with atherosclerosis. Recent studies have demonstrated that HDL mediates the transport of cholesterol from peripheral tissues to the liver through “reverse cholesterol transport” pathway. However there is considerable debate about the mechanisms by which HDL removes excess cholesterol from cells. Two different pathways were suggested: (i) a docking receptor promoting cholesterol transl

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8

Getz, Godfrey, and Catherine Reardon. "Apoprotein E and Reverse Cholesterol Transport." International Journal of Molecular Sciences 19, no. 11 (2018): 3479. http://dx.doi.org/10.3390/ijms19113479.

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Apoprotein E (apoE) is a multifunctional protein. Its best-characterized function is as a ligand for low-density lipoprotein (LDL) receptor family members to mediate the clearance of apoB-containing atherogenic lipoproteins. Among its other functions, apoE is involved in cholesterol efflux, especially from cholesterol-loaded macrophage foam cells and other atherosclerosis-relevant cells, and in reverse cholesterol transport. Reverse cholesterol transport is a mechanism by which excess cellular cholesterol is transported via lipoproteins in the plasma to the liver where it can be excreted from

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9

Motte, Alexandre, Julie Gall, Joe-Elie Salem, et al. "Reduced Reverse Cholesterol Transport Efficacy in Healthy Men with Undesirable Postprandial Triglyceride Response." Biomolecules 10, no. 5 (2020): 810. http://dx.doi.org/10.3390/biom10050810.

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Elevation of nonfasting triglyceride (TG) levels above 1.8 g/L (2 mmol/L) is associated with increased risk of cardiovascular diseases. Exacerbated postprandial hypertriglyceridemia (PP–HTG) and metabolic context both modulate the overall efficacy of the reverse cholesterol transport (RCT) pathway, but the specific contribution of exaggerated PP–HTG on RCT efficacy remains indeterminate. Healthy male volunteers (n = 78) exhibiting no clinical features of metabolic disorders underwent a postprandial exploration following consumption of a typical Western meal providing 1200 kcal. Subjects were s

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10

Weingärtner, Oliver, Ulrich Laufs, Michael Böhm, and Dieter Lütjohann. "An alternative pathway of reverse cholesterol transport: The oxysterol 27-hydroxycholesterol." Atherosclerosis 209, no. 1 (2010): 39–41. http://dx.doi.org/10.1016/j.atherosclerosis.2009.09.015.

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Chao, W. T., and V. C. Yang. "Role of Plasmalemmal Vesicles on the HDL-Mediated Cholesterol Efflux in Aortic Endothelial Cells." Microscopy and Microanalysis 7, S2 (2001): 644–45. http://dx.doi.org/10.1017/s1431927600029299.

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It is well-known that high-density lipoprotein (HDL) mediates the transport of cholesterol from peripheral tissues to liver through “reverse cholesterol transport” for metabolism. However there is considerable debate about the mechanisms by which HDL removes excess cholesterol from cells. Two different pathways have been suggested: (i) a docking receptor promots cholesterol translocation, or (ii) a receptor mediates intracellular endosomal pathway termed “retroendocytosis“. Our previous studies have indicated that the removal of cholesterol from aortic endothelial and smooth muscle cells in th

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12

Ren, Kun, Ting Jiang та Guo-Jun Zhao. "Quercetin induces the selective uptake of HDL-cholesterol via promoting SR-BI expression and the activation of the PPARγ/LXRα pathway". Food & Function 9, № 1 (2018): 624–35. http://dx.doi.org/10.1039/c7fo01107e.

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Reverse cholesterol transport (RCT) is the process to deliver cholesterol to the liver for further excretion and involves scavenger receptor class B type I (SR-BI)-mediated selective lipid uptake (SLU) from high-density lipoprotein cholesterol (HDL-C).

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Crestani, M., E. De Fabiani, D. Caruso, et al. "LXR (liver X receptor) and HNF-4 (hepatocyte nuclear factor-4): key regulators in reverse cholesterol transport." Biochemical Society Transactions 32, no. 1 (2004): 92–96. http://dx.doi.org/10.1042/bst0320092.

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Cholesterol homoeostasis is the result of the fine tuning between intake and disposal of this molecule. High levels of cholesterol in the blood are detrimental as they may lead to excessive accumulation in vessel walls, a condition predisposing to the development of atherosclerotic lesions. Cholesterol is removed from the vessel wall and transported to the liver through a process called reverse cholesterol transport. Nuclear receptors are among the most important transcription factors regulating genes involved in different steps of reverse cholesterol transport. Here, we discuss the role of th

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LIE, Jessica, Rini de CROM, Matti JAUHIAINEN та ін. "Evaluation of phospholipid transfer protein and cholesteryl ester transfer protein as contributors to the generation of preβ-high-density lipoproteins". Biochemical Journal 360, № 2 (2001): 379–85. http://dx.doi.org/10.1042/bj3600379.

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High-density lipoproteins (HDLs) are considered anti-atherogenic because they mediate peripheral cell cholesterol transport to the liver for excretion and degradation. An important step in this reverse cholesterol-transport pathway is the uptake of cellular cholesterol by a specific subclass of small, lipid-poor apolipoprotein A-I particles designated preβ-HDL. The two lipid-transfer proteins present in human plasma, cholesteryl ester transfer protein (CETP) and phospholipid transfer protein (PLTP), have both been implicated in the formation of preβ-HDL. In order to investigate the relative co

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15

Li, Tiangang, and John Y. L. Chiang. "Regulation of Bile Acid and Cholesterol Metabolism by PPARs." PPAR Research 2009 (2009): 1–15. http://dx.doi.org/10.1155/2009/501739.

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Bile acids are amphipathic molecules synthesized from cholesterol in the liver. Bile acid synthesis is a major pathway for hepatic cholesterol catabolism. Bile acid synthesis generates bile flow which is important for biliary secretion of free cholesterol, endogenous metabolites, and xenobiotics. Bile acids are biological detergents that facilitate intestinal absorption of lipids and fat-soluble vitamins. Recent studies suggest that bile acids are important metabolic regulators of lipid, glucose, and energy homeostasis. Agonists of peroxisome proliferator-activated receptors (PPARα, PPARγ, PPA

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16

Cedó, Lídia, Jari Metso, David Santos, et al. "LDL Receptor Regulates the Reverse Transport of Macrophage-Derived Unesterified Cholesterol via Concerted Action of the HDL-LDL Axis." Circulation Research 127, no. 6 (2020): 778–92. http://dx.doi.org/10.1161/circresaha.119.316424.

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Rationale: The HDL (high-density lipoprotein)-mediated stimulation of cellular cholesterol efflux initiates macrophage-specific reverse cholesterol transport (m-RCT), which ends in the fecal excretion of macrophage-derived unesterified cholesterol (UC). Early studies established that LDL (low-density lipoprotein) particles could act as efficient intermediate acceptors of cellular-derived UC, thereby preventing the saturation of HDL particles and facilitating their cholesterol efflux capacity. However, the capacity of LDL to act as a plasma cholesterol reservoir and its potential impact in supp

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17

Jiménez-Cortegana, Carlos, Soledad López-Enríquez, Gonzalo Alba, et al. "The Expression of Genes Related to Reverse Cholesterol Transport and Leptin Receptor Pathways in Peripheral Blood Mononuclear Cells Are Decreased in Morbid Obesity and Related to Liver Function." International Journal of Molecular Sciences 25, no. 14 (2024): 7549. http://dx.doi.org/10.3390/ijms25147549.

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Obesity is frequently accompanied by non-alcoholic fatty liver disease (NAFLD). These two diseases are associated with altered lipid metabolism, in which reverse cholesterol transport (LXRα/ABCA1/ABCG1) and leptin response (leptin receptor (Ob-Rb)/Sam68) are involved. The two pathways were evaluated in peripheral blood mononuclear cells (PBMCs) from 86 patients with morbid obesity (MO) before and six months after Roux-en-Y gastric bypass (RYGB) and 38 non-obese subjects. In the LXRα pathway, LXRα, ABCA1, and ABCG1 mRNA expressions were decreased in MO compared to non-obese subjects (p < 0.0

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18

Graham, Annette, Dimitri V. Vinogradov, and James S. Owen. "Effects of peroxynitrite on plasma components of the reverse cholesterol transport pathway." FEBS Letters 431, no. 3 (1998): 327–32. http://dx.doi.org/10.1016/s0014-5793(98)00785-6.

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Bernecic, Naomi C., Simon P. de Graaf, Tamara Leahy, and Bart M. Gadella. "HDL mediates reverse cholesterol transport from ram spermatozoa and induces hyperactivated motility." Biology of Reproduction 104, no. 6 (2021): 1271–81. http://dx.doi.org/10.1093/biolre/ioab035.

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Abstract Reverse cholesterol transport or cholesterol efflux is part of an extensive plasma membrane remodeling process in spermatozoa that is imperative for fertilization. For ram spermatozoa, sheep serum is well known to support in vitro fertilization (IVF), but knowledge of its explicit role is limited. Though, it is postulated to elicit cholesterol efflux owing to the presence of high-density lipoproteins (HDLs) that interact with transmembrane cholesterol transporters, such as adenosinetriphosphate (ATP)-binding cassette transporter A1 (ABCA1) and scavenger receptor class B, type I (SR-BI

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20

Berrougui, Hicham, Souad Ikhlef, and Abdelouahed Khalil. "Extra Virgin Olive Oil Polyphenols Promote Cholesterol Efflux and Improve HDL Functionality." Evidence-Based Complementary and Alternative Medicine 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/208062.

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Results of the present work give evidence from the beneficial role of extra virgin olive of oil (EVOO) consumption towards oxidative stress and cardiovascular diseases. Polyphenols contained in EVOO are responsible for inhibiting lipoproteins oxidative damages and promoting reverse cholesterol transport process via ABCA1 pathway.

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Orsoni, Alexina, Elise F. Villard, Eric Bruckert, et al. "Impact of LDL apheresis on atheroprotective reverse cholesterol transport pathway in familial hypercholesterolemia." Journal of Lipid Research 53, no. 4 (2012): 767–75. http://dx.doi.org/10.1194/jlr.m024141.

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Liu, Jichen, Kai Guo, Lu Hu, et al. "ZAP70 deficiency promotes reverse cholesterol transport through MAPK/ERK pathway in Jurkat cell." Molecular Immunology 107 (March 2019): 21–28. http://dx.doi.org/10.1016/j.molimm.2019.01.001.

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Uto-Kondo, Harumi, Makoto Ayaori, Grace Megumi Sotherden, et al. "Ezetimibe enhances macrophage reverse cholesterol transport in hamsters: Contribution of hepato–biliary pathway." Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids 1841, no. 9 (2014): 1247–55. http://dx.doi.org/10.1016/j.bbalip.2014.05.009.

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Huang, Zhiping, Akihiro Inazu, Masa-aki Kawashiri, Atsushi Nohara, Toshinori Higashikata, and Hiroshi Mabuchi. "Dual effects on HDL metabolism by cholesteryl ester transfer protein inhibition in HepG2 cells." American Journal of Physiology-Endocrinology and Metabolism 284, no. 6 (2003): E1210—E1219. http://dx.doi.org/10.1152/ajpendo.00453.2002.

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Cholesteryl ester transfer protein (CETP) promotes reverse cholesterol transport via exchange of cholesteryl ester and triglyceride among lipoproteins. Here, we focused on HDL metabolism during inhibition of CETP expression by using CETP antisense oligodeoxynucleotides (ODNs) in HepG2 cells. CETP secretion was decreased by 70% in mRNA levels and by 52% in mass 20 h after ODNs against CETP were delivered to HepG2 cells. Furthermore, as a consequence of the downregulation of CETP, the expression of scavenger receptor class B type I (SR-BI), an HDL receptor, was also reduced by ∼50% in mRNA and p

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Peterson, Stephen J., Abu Choudhary, Amardeep K. Kalsi, Shuyang Zhao, Ragin Alex, and Nader G. Abraham. "OX-HDL: A Starring Role in Cardiorenal Syndrome and the Effects of Heme Oxygenase-1 Intervention." Diagnostics 10, no. 11 (2020): 976. http://dx.doi.org/10.3390/diagnostics10110976.

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In this review, we will evaluate how high-density lipoprotein (HDL) and the reverse cholesterol transport (RCT) pathway are critical for proper cardiovascular–renal physiology. We will begin by reviewing the basic concepts of HDL cholesterol synthesis and pathway regulation, followed by cardiorenal syndrome (CRS) pathophysiology. After explaining how the HDL and RCT pathways become dysfunctional through oxidative processes, we will elaborate on the potential role of HDL dysfunction in CRS. We will then present findings on how HDL function and the inducible antioxidant gene heme oxygenase-1 (HO

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Gautier, Thomas, and Laurent Lagrost. "Plasma PLTP (phospholipid-transfer protein): an emerging role in ‘reverse lipopolysaccharide transport’ and innate immunity." Biochemical Society Transactions 39, no. 4 (2011): 984–88. http://dx.doi.org/10.1042/bst0390984.

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Plasma PLTP (phospholipid-transfer protein) is a member of the lipid transfer/LBP [LPS (lipopolysaccharide)-binding protein] family, which constitutes a superfamily of genes together with the short and long PLUNC (palate, lung and nasal epithelium clone) proteins. Although PLTP was studied initially for its involvement in the metabolism of HDL (high-density lipoproteins) and reverse cholesterol transport (i.e. the metabolic pathway through which cholesterol excess can be transported from peripheral tissues back to the liver for excretion in the bile), it displays a number of additional biologi

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Aron-Wisnewsky, Judith, Zélie Julia, Christine Poitou, et al. "Effect of Bariatric Surgery-Induced Weight Loss on SR-BI-, ABCG1-, and ABCA1-Mediated Cellular Cholesterol Efflux in Obese Women." Journal of Clinical Endocrinology & Metabolism 96, no. 4 (2011): 1151–59. http://dx.doi.org/10.1210/jc.2010-2378.

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Abstract Aim: We tested the hypothesis that quantitative changes in high-density lipoprotein (HDL) particles weight loss induced by Roux-en-Y bypass (RYGBP) in morbidly obese subjects might be associated with improved functionality of these particles in the reverse cholesterol transport pathway. Methods and Results: Thirty-four morbidly obese women were recruited and followed up before and 6 months after RYGBP. After surgery, along with a major weight loss (−20%; P &lt; 0.0001), we observed a significant increase in HDL mass concentration (+14%; P &lt; 0.04), reflecting a specific incr

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Greco, Daniela, Simone Battista, Laura Mele, et al. "Alcohol Pattern Consumption Differently Affects the Efficiency of Macrophage Reverse Cholesterol Transport in Vivo." Nutrients 10, no. 12 (2018): 1885. http://dx.doi.org/10.3390/nu10121885.

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It has been well established that moderate alcohol consumption inversely correlates with cardiovascular morbidity and mortality, whereas binge alcohol drinking increases cardiovascular disease risk. The aim of this study was to assess in vivo the impact of different drinking patterns on reverse cholesterol transport (RCT); the atheroprotective process leading to the removal of excess cholesterol from the body. RCT was measured with a standardized, radioisotope-based technique in three groups of atherosclerosis-prone apolipoprotein E knock out mice: Placebo group, receiving water, which would m

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Li, Zhonghao, Qi Zhang, Xianyan Liu та Ming Zhao. "Recombinant Humanized IgG1 Antibody Promotes Reverse Cholesterol Transport through FcRn-ERK1/2-PPARα Pathway in Hepatocytes". International Journal of Molecular Sciences 23, № 23 (2022): 14607. http://dx.doi.org/10.3390/ijms232314607.

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Hyperlipidemia-associated lipid disorders are considered the cause of atherosclerotic cardiovascular disease. Reverse cholesterol transport (RCT) is a mechanism by which excess peripheral cholesterol is transported to the liver and further converted into bile acid for excretion from the body in feces, which contributes to reducing hyperlipidemia as well as cardiovascular disease. We previously found that the recombinant humanized IgG1 antibody promotes macrophages to engulf lipids and increases cholesterol efflux to high-density lipoprotein (HDL) through ATP-binding cassette sub-family A1 (ABC

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Ali, A., and I. Asghar. "003 Stimulate Reverse Cholesterol Transport Pathway By Increasing the Negative Surface Potential of HDL." Canadian Journal of Cardiology 28, no. 5 (2012): S84. http://dx.doi.org/10.1016/j.cjca.2012.07.017.

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Xie, Jing, Li Peng, Taotao wang та ін. "QiShenYiQi pill inhibits atherosclerosis by promoting reverse cholesterol transport PPARγ-LXRα/β-ABCA1 pathway". Journal of Ethnopharmacology 315 (жовтень 2023): 116684. http://dx.doi.org/10.1016/j.jep.2023.116684.

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Park, Sin-Hye, and Young-Hee Kang. "Dietary Ellagic Acid Ameliorates Functionality of Reverse Cholesterol Transport in apoE-Deficient Mice." Current Developments in Nutrition 6, Supplement_1 (2022): 325. http://dx.doi.org/10.1093/cdn/nzac053.066.

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Abstract Objectives High levels of plasma LDL cholesterol are an important determinant of atherosclerotic lesion formation. The disruption of the process of cholesterol efflux or reverse cholesterol transport (RCT) of peripheral cells may promote atherogenesis. The aim of the current study was to investigate whether ellagic acid alleviated atherosclerotic development through activating RCT pathway in apoE knockout (KO) mice. Methods Wild type mice and apoE KO mice were fed high-fat high-cholesterol Paigen's diets for 10 weeks to induce hypercholesterolemia and atherosclerosis, and concomitantl

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de Beer, Maria C., Joanne M. Wroblewski, Victoria P. Noffsinger, et al. "The Impairment of Macrophage-to-Feces Reverse Cholesterol Transport during Inflammation Does Not Depend on Serum Amyloid A." Journal of Lipids 2013 (2013): 1–11. http://dx.doi.org/10.1155/2013/283486.

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Studies suggest that inflammation impairs reverse cholesterol transport (RCT). We investigated whether serum amyloid A (SAA) contributes to this impairment using an established macrophage-to-feces RCT model. Wild-type (WT) mice and mice deficient in SAA1.1 and SAA2.1 (SAAKO) were injected intraperitoneally with3H-cholesterol-labeled J774 macrophages 4 hr after administration of LPS or buffered saline.3H-cholesterol in plasma 4 hr after macrophage injection was significantly reduced in both WT and SAAKO mice injected with LPS, but this was not associated with a reduced capacity of serum from LP

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Lee-Rueckert, Miriam, Reija Silvennoinen, Noemi Rotllan, et al. "Mast Cell Activation In Vivo Impairs the Macrophage Reverse Cholesterol Transport Pathway in the Mouse." Arteriosclerosis, Thrombosis, and Vascular Biology 31, no. 3 (2011): 520–27. http://dx.doi.org/10.1161/atvbaha.110.221069.

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Wang, Ming-Dong, Robert S. Kiss, Vivian Franklin, Heidi M. McBride, Stewart C. Whitman, and Yves L. Marcel. "Different cellular traffic of LDL-cholesterol and acetylated LDL-cholesterol leads to distinct reverse cholesterol transport pathways." Journal of Lipid Research 48, no. 3 (2006): 633–45. http://dx.doi.org/10.1194/jlr.m600470-jlr200.

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Chen, Xuemeng, Kun Tang, Yi Peng та XiaoLe Xu. "2,3,4′,5-tetrahydroxystilbene-2-O-β-d-glycoside attenuates atherosclerosis in apolipoprotein E-deficient mice: role of reverse cholesterol transport". Canadian Journal of Physiology and Pharmacology 96, № 1 (2018): 8–17. http://dx.doi.org/10.1139/cjpp-2017-0474.

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The aim of this study was to evaluate the potential effects of 2,3,4′,5-tetrahydroxystilbene-2-O-β-d-glucoside (TSG) on the development of atherosclerotic plaque in ApoE−/− mice, and explore the mechanisms involved. Our data showed that after 8 weeks of treatment, TSG ameliorated serum levels of total cholesterol, triglyceride, and low density lipoprotein cholesterol, and increased serum levels of high density lipoprotein cholesterol in ApoE−/− mice. TSG suppressed hepatic steatosis, the formation of atherosclerotic lesions, and the formation of macrophage foam cells in ApoE−/− mice. Moreover,

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Endo-Umeda, Kaori, and Makoto Makishima. "Liver X Receptors Regulate Cholesterol Metabolism and Immunity in Hepatic Nonparenchymal Cells." International Journal of Molecular Sciences 20, no. 20 (2019): 5045. http://dx.doi.org/10.3390/ijms20205045.

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Excess dietary cholesterol intake and the dysregulation of cholesterol metabolism are associated with the pathogenesis and progression of nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, and fibrosis. Hepatic accumulation of free cholesterol induces activation of nonparenchymal cells, including Kupffer cells, macrophages, and hepatic stellate cells, which leads to persistent inflammation and fibrosis. The nuclear receptors liver X receptor α (LXRα) and LXRβ act as negative regulators of cholesterol metabolism through the induction of hepatocyte cholesterol catabolism, excretion,

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Tabet, Fatiha, and Kerry-Anne Rye. "High-density lipoproteins, inflammation and oxidative stress." Clinical Science 116, no. 2 (2008): 87–98. http://dx.doi.org/10.1042/cs20080106.

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Plasma levels of HDL (high-density lipoprotein)-cholesterol are strongly and inversely correlated with atherosclerotic cardiovascular disease. Both clinical and epidemiological studies have reported an inverse and independent association between serum HDL-cholesterol levels and CHD (coronary heart disease) risk. The cardioprotective effects of HDLs have been attributed to several mechanisms, including their involvement in the reverse cholesterol transport pathway. HDLs also have antioxidant, anti-inflammatory and antithrombotic properties and promote endothelial repair, all of which are likely

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Silvennoinen, R., M. Lee-Rueckert, N. Rotllan, et al. "190 MAST CELL ACTIVATION IN VIVO IMPAIRS THE MACROPHAGE REVERSE CHOLESTEROL TRANSPORT PATHWAY IN THE MOUSE." Atherosclerosis Supplements 12, no. 1 (2011): 42. http://dx.doi.org/10.1016/s1567-5688(11)70191-x.

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조진경, 진영윤, 홍혜련, et al. "Effects of Exercise on Genes Expression of the Reverse Cholesterol Transport Pathway in Middle-Aged Women." Exercise Science 21, no. 1 (2012): 59–68. http://dx.doi.org/10.15857/ksep.2012.21.1.59.

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Remaley, A. T. "“Who's on First”: Determining the roster for the key players in the reverse cholesterol transport pathway." Atherosclerosis 218, no. 2 (2011): 287–89. http://dx.doi.org/10.1016/j.atherosclerosis.2011.06.037.

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Chambers, Karen F., Priscilla E. Day, Hassan T. Aboufarrag, and Paul A. Kroon. "Polyphenol Effects on Cholesterol Metabolism via Bile Acid Biosynthesis, CYP7A1: A Review." Nutrients 11, no. 11 (2019): 2588. http://dx.doi.org/10.3390/nu11112588.

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Atherosclerosis, the main contributor to coronary heart disease, is characterised by an accumulation of lipids such as cholesterol in the arterial wall. Reverse cholesterol transport (RCT) reduces cholesterol via its conversion into bile acids (BAs). During RCT in non-hepatic peripheral tissues, cholesterol is transferred to high-density lipoprotein (HDL) particles and returned to the liver for conversion into BAs predominantly via the rate-limiting enzyme, cholesterol 7 α-hydroxylase (CYP7A1). Numerous reports have described that polyphenol induced increases in BA excretion and corresponding

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Dullaart, Robin P. F., Albert K. Groen, Geesje M. Dallinga-Thie, Rindert de Vries, Wim J. Sluiter, and Arie van Tol. "Fibroblast cholesterol efflux to plasma from metabolic syndrome subjects is not defective despite low high-density lipoprotein cholesterol." European Journal of Endocrinology 158, no. 1 (2008): 53–60. http://dx.doi.org/10.1530/eje-07-0451.

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ObjectiveWe tested whether in metabolic syndrome (MetS) subjects the ability of plasma to stimulate cellular cholesterol efflux, an early step in the anti-atherogenic reverse cholesterol transport pathway, is maintained despite low high-density lipoprotein (HDL) cholesterol.DesignIn 76 subjects with and 94 subjects without MetS based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, we determined plasma (apo)lipoproteins, pre-β-HDL formation, phospholipid transfer protein (PLTP) activity, cholesterol esterification (EST), cholesteryl ester transfe

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Turner, S., J. Voogt, J. Luchoomun та ін. "Abstract: P1442 EFFECT OF PPARΔ TREATMENT ON PATHWAYS OF REVERSE CHOLESTEROL TRANSPORT". Atherosclerosis Supplements 10, № 2 (2009): e1492. http://dx.doi.org/10.1016/s1567-5688(09)71450-3.

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D’Amore, Simona, Jennifer Härdfeldt, Marica Cariello, et al. "Identification of miR-9-5p as direct regulator of ABCA1 and HDL-driven reverse cholesterol transport in circulating CD14+ cells of patients with metabolic syndrome." Cardiovascular Research 114, no. 8 (2018): 1154–64. http://dx.doi.org/10.1093/cvr/cvy077.

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Abstract Aims Metabolic syndrome (MS) is a cluster of cardio-metabolic risk factors associated with atherosclerosis and low-grade inflammation. Using unbiased expression screenings in peripheral blood mononuclear cells, we depict here a novel expression chart of 678 genes and 84 microRNAs (miRNAs) controlling inflammatory, immune and metabolic responses. In order to further elucidate the link between inflammation and the HDL cholesterol pathway in MS, we focussed on the regulation of the ATP-binding cassette transporter A1 (ABCA1), a key player in cholesterol efflux (CE). Methods and results A

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Catalano, Giovanna, Zélie Julia, Eric Frisdal, et al. "Torcetrapib Differentially Modulates the Biological Activities of HDL2 and HDL3 Particles in the Reverse Cholesterol Transport Pathway." Arteriosclerosis, Thrombosis, and Vascular Biology 29, no. 2 (2009): 268–75. http://dx.doi.org/10.1161/atvbaha.108.179416.

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CHABANE, Fatima, Nabila Boukhari Benahmed Daidj, Sabrine LOUALA, and Myriem Lamri Senhadji. "Effect of Silybum marianum (L. Gaerthn) on C-reactive protein, Lactate Dehydrogenase and Reverse Cholesterol Transport in Rats Prematurely Exposed to a High-Fat, High-Sugar Diet." South Asian Journal of Experimental Biology 12, no. 6 (2022): 789–99. http://dx.doi.org/10.38150/sajeb.12(6).p789-799.

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The milk thistle (Silybum marianum (Sm)) is a medicinal plant used for a long time in the Algerian traditional medicine. its cardioprotective and preventive effects against the development of obesity complications have been very little investigated. The aim of this study was to see if milk thistle seed can slow down the onset of cardio-metabolic disorders in rats prematurely exposed to a High Lipid/High Sugar (HL/HS) diet. Thirty male Wistar rats are divided into three homogeneous groups. The first Control group (C) receives a normocaloric diet; the second consumes the HL/HS diet (untreated gr

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Shao, Baohai, Xiaoyun Fu, Thomas O. McDonald, et al. "Acrolein Impairs ATP Binding Cassette Transporter A1-dependent Cholesterol Export from Cells through Site-specific Modification of Apolipoprotein A-I." Journal of Biological Chemistry 280, no. 43 (2005): 36386–96. http://dx.doi.org/10.1074/jbc.m508169200.

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Acrolein is a highly reactive α,β-unsaturated aldehyde, but the factors that control its reactions with nucleophilic groups on proteins remain poorly understood. Lipid peroxidation and threonine oxidation by myeloperoxidase are potential sources of acrolein during inflammation. Because both pathways are implicated in atherogenesis and high density lipoprotein (HDL) is anti-atherogenic, we investigated the possibility that acrolein might target the major protein of HDL, apolipoprotein A-I (apoA-I), for modification. Tandem mass spectrometric analysis demonstrated that lysine 226, located near t

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Kotlyarov, Stanislav. "Genetic and Epigenetic Regulation of Lipoxygenase Pathways and Reverse Cholesterol Transport in Atherogenesis." Genes 13, no. 8 (2022): 1474. http://dx.doi.org/10.3390/genes13081474.

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Atherosclerosis is one of the most important medical and social problems of modern society. Atherosclerosis causes a large number of hospitalizations, disability, and mortality. A considerable amount of evidence suggests that inflammation is one of the key links in the pathogenesis of atherosclerosis. Inflammation in the vascular wall has extensive cross-linkages with lipid metabolism, and lipid mediators act as a central link in the regulation of inflammation in the vascular wall. Data on the role of genetics and epigenetic factors in the development of atherosclerosis are of great interest.

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Zhang, Zhexiao, Yunmei Qiu, Wanzhi Li, et al. "Astaxanthin Alleviates Foam Cell Formation and Promotes Cholesterol Efflux in Ox-LDL-Induced RAW264.7 Cells via CircTPP2/miR-3073b-5p/ABCA1 Pathway." Molecules 28, no. 4 (2023): 1701. http://dx.doi.org/10.3390/molecules28041701.

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Atherosclerosis (AS) is a common cardiovascular disease and remains the leading cause of death in the world. It is generally believed that the deposition of foam cells in the arterial wall is the main cause of AS. Moreover, promoting cholesterol efflux and enhancing the ability of reverse cholesterol transport (RCT) can effectively inhibit the formation of foam cells, thereby preventing the occurrence and development of AS. Astaxanthin, with a powerful antioxidant ability, has a potential role in the prevention of atherosclerosis, but how it works in preventing atherosclerosis remains unknown.

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