Foam cells in atherosclerosis.
By Xiao-Hua Yu, Yu-chang Fu, Da-wei Zhang, Kai Yin, Chao-ke Tang. Clinica chimica acta; international journal of clinical chemistry, 2013
739 citations recorded by the source corpus.
Atherosclerosis is a chronic disease characterized by the deposition of excessive cholesterol in the arterial intima. Macrophage foam cells play a critical role in the occurrence and development of atherosclerosis. The generation of these cells is associated with imbalance of cholesterol influx, esterification and efflux. CD36 and scavenger receptor class A (SR-A) are mainly responsible for uptake of lipoprotein-derived cholesterol by macrophages. Acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1) and neutral cholesteryl ester hydrolase (nCEH) regulate cholesterol esterification. ATP-binding cassette transporters A1(ABCA1), ABCG1 and scavenger receptor BI (SR-BI) play crucial roles in macrophage cholesterol export. When inflow and esterification of cholesterol increase and/or its outflow decrease, the macrophages are ultimately transformed into lipid-laden foam cells, the prototypical cells in the atherosclerotic plaque. The aim of this review is to describe what is known about the mechanisms of cholesterol uptake, esterification and release in macrophages. An increased understanding of the process of macrophage foam cell formation will help to develop novel therapeutic interventions for atherosclerosis.
Subfields: Cancer Research, Immunology, Surgery
View Paper: https://www.semanticscholar.org/paper/7f4b62d7960d97fa71842f260135508f1c5a63ad
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Citations in the corpus
- Pathophysiology of Atherosclerosis (2022, background): “Modified LDLs are avidly captured by differentiated monocytes and VSMC, which promote foam cell formation [19,20].”
- Mechanisms of foam cell formation in atherosclerosis (2017, background): “have an advanced enzymatic machinery, such as acyl coenzyme A:cholesterol acyltransferase-1 (ACAT1), which is essential for formation of cholesterol esters [8].”