Cor Vasa 2024, 66(1):66-70 | DOI: 10.33678/cor.2024.005

(The CD36 receptor - the link between inflammation, lipid metabolism, and cardiovascular disease)

Rudolf Poledne, Ivana Králová Lesná

Laboratoř pro výzkum aterosklerózy, Centrum experimentální medicíny, Institut klinické a experimentální medicíny, Praha, Česká republika

The CD36/FAT (fatty acid translocator) receptor is a crucial player in cardiovascular diseases, featuring a consistent structure across species. Its expression in adipose tissue, skeletal muscle, liver, and arterial wall macrophages underscores its importance. Beyond scavenging oxidized LDL (oxLDL), CD36 accelerates the pro-inflammatory processes in all these organs. Specific microenvironments of adipose tissue with high concentrations of free long-chain fatty acids, insulin, and glucose induce polarization by tissue-specific path- ways producing metabolically activated pro-inflammatory macrophages (MAPIMs) with high CD36 expres- sion. The proportion of MAPIMs in human adipose tissue correlates significantly with the two main risk predictors of cardiovascular diseases - hypercholesterolemia and obesity. Polarization of MAPIMs in adipose tissue is defined by the fatty acid composition of cell membrane phospholipids, and increases with the proportion of palmitic, and mainly palmitoleate, fatty acids and decreases with the presence of n-3 polyenic fatty acids, specifically α-linolenic and eicosapentaenoic fatty acids. When analysing this effect separately for adipocytes and macrophages, we found that adipocytes create a microenvironment (with a relationship similar to the effects of individual fatty acids of membrane phospholipids) beneficial for pro-inflammatory polarization. On the contrary, macrophage polarization is related to the competition of unsaturated palmitate and cholesterol molecules in the membrane raft. CD36 is crucial for the development of atherosclerosis within the arterial wall, scavenging oxLDL producing fatty streaks and foam cells until the formation of complicated atherosclerotic lesions. CD36 deficiency attenuates atherosclerotic lesion development both in experimental models and individuals with genetic defects of this receptor. The complex role of CD36 in inflammation, lipid metabolism, and angiogenesis makes it a key player in cell- and organ-level communication, activating the atherogenic process.

Keywords: Atherosclerosis, CD36 receptor, Inflammation

Received: January 9, 2024; Revised: January 9, 2024; Accepted: January 10, 2024; Prepublished online: June 2, 2012; Published: March 5, 2024  Show citation