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Platelet glycoprotein 4 (CD36), also known as Fatty acid translocase (FAT), is a multifunctional class B scavenger receptor expressed on various cell types, including microvascular endothelial cells, macrophages, and adipocytes (1, 2). On endothelial cells, CD36 serves as a critical negative regulator of angiogenesis by binding to thrombospondin-1 (TSP-1), which triggers a signaling cascade involving Fyn, p38 MAPK, and JNK that leads to endothelial cell apoptosis (6, 13). Beyond its role in vascular biology, CD36 facilitates the high-affinity uptake of long-chain fatty acids and oxidized low-density lipoproteins (oxLDL), making it a central player in lipid metabolism and the development of atherosclerosis (10, 17). In oncology, CD36 is increasingly recognized for its role in promoting cancer metastasis and providing metabolic support to tumor cells through lipid uptake (15, 19). Therapeutic strategies targeting CD36 include TSP-1 mimetics to inhibit tumor angiogenesis and small molecule inhibitors to block fatty acid transport in metabolic and cardiovascular diseases (9, 15).
Inhibition of angiogenesis via thrombospondin-1 mimetic binding, modulation of long-chain fatty acid uptake, and inhibition of inflammatory signaling pathways triggered by oxidized LDL.
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