Cd36, also known as the scavenger receptor B2, is a multifunctional transmembrane glycoprotein. It plays a crucial role in the uptake of long-chain fatty acids, acting as a key regulator of lipid metabolism. It is involved in various processes such as immunological recognition, inflammation, molecular adhesion, and apoptosis. Its post-translational modifications, including phosphorylation, ubiquitination, glycosylation, and palmitoylation, regulate its maturation and transportation [1,3,7].

In cardiovascular diseases, Cd36 deficiency alleviates diabetic cardiomyopathy and atherosclerosis, while overexpression eliminates ischemia-reperfusion damage, suggesting its close association with disease progression [1]. In metabolic disorders, it is a critical fatty acid sensor and regulator, and its interaction with lipid dysmetabolism and obesity has been identified [2]. In cancer, Cd36 has a complex role, both promoting and inhibiting cancer progression. It mediates lipid uptake to fuel tumor metastasis and therapy resistance, yet attenuates angiogenesis by binding to thrombospondin-1 [3,4,6]. In chronic kidney disease, antagonist blockade or genetic knockout of Cd36 prevents kidney injury, indicating its potential as a therapeutic target [5].

In conclusion, Cd36 is essential for lipid metabolism and is involved in multiple disease processes. Gene knockout (KO) and conditional knockout (CKO) mouse models have been instrumental in revealing its role in cardiovascular diseases, metabolic disorders, cancer, and chronic kidney disease, providing potential therapeutic targets for these diseases.