Abstract
Atherosclerosis is a progressive, chronic inflammation in artery walls. Oxidized low density lipoproteins (ox-LDL) play an important role in atherosclerotic plaque formation. ox-LDL are taken up by macrophages mainly through scavenger receptors, among which CD36 is considered to be the most important. Animal studies have shown that crossing atherogenic mice with a strain lacking the expression of CD36 prevented the development of atherosclerosis despite a diet rich in saturated LCFA. In humans, autopsy studies performed in obese patients have demonstrated increased expression of CD36 receptor on macrophages, comprised within atherosclerotic plaques. Until recently it had been believed that CD36 is a major player in atherosclerosis progression in humans. However, recent studies challenge this conviction, showing increased incidence of coronary heart disease in the subgroup of patients with decreased expression of CD36. This article reviews the role of CD36 receptor in the development of atherosclerosis. The authors also discuss current possibilities to interfere with CD36, their potential benefits and hazards.
Highlights
This study suggests that CD36 takes part in the development of atherosclerosis by regulating the intracellular influx of calcium and synthesis of prostaglandin E2 from arachidonic acid
CD36 is a major protein involved in Oxidized low density lipoproteins (ox-LDL) uptake into macrophages
Animal studies suggest an important role of CD36 receptor in the development of atherosclerosis
Summary
Lack of the lipid component of ox-LDLs inhibits their uptake by CD36 receptor and, as a result, reduces lipoprotein accumulation in macrophages.[2] After entering monocytes or macrophages, LCFA are bound by cytoplasmic fatty acid binding proteins (FABPc) and depending on the needs of the cell, they are targeted to suitable intracellular locations for rendering: oxidation in mitochondria and peroxisomes or storage (mainly esterified) in the endoplasmic reticulum and the cytoplasm.[9]
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