CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications

Area of Science:

• Cardiovascular Biology
• Immunology
• Metabolic Disease

Background:

• Atherosclerosis involves lipid retention and inflammation in artery walls, driven by modified low-density lipoprotein (LDL).
• Oxidized LDL (ox-LDL) uptake by cells via scavenger receptors like CD36 is critical in plaque development.
• CD36 is a scavenger receptor and signaling hub involved in lipid and inflammatory pathways.

Purpose of the Study:

• To review the structure, ligands, functions, and regulation of CD36 in atherosclerosis.
• To focus on the pathological role of CD36 in endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets.
• To highlight therapeutic strategies targeting CD36 for atherosclerosis.

Main Methods:

• State-of-the-art literature review.
• Analysis of CD36's role in cellular dysfunction.
• Examination of CD36's involvement in lipid and inflammatory pathways.

Main Results:

• CD36 deficiency in mice suggests a protective role against atherosclerosis.
• Soluble CD36 levels are elevated in patients with atherosclerosis and metabolic disorders.
• CD36 mediates ox-LDL uptake and contributes to cellular dysfunction in atherosclerosis.

Conclusions:

• CD36 is a significant contributor to atherosclerotic plaque formation and progression.
• Targeting CD36 expression or activity presents a promising therapeutic avenue for atherosclerosis.
• Further research into CD36's multifaceted roles can advance cardiovascular disease treatment.