CD36 (also known as scavenger receptor B2) is a multifunctional receptor that mediates the binding and cellular uptake of long-chain fatty acids, oxidized lipids and phospholipids, advanced oxidation protein products, thrombospondin and advanced glycation end products, and has roles in lipid accumulation, inflammatory signalling, energy reprogramming, apoptosis and kidney fibrosis. Renal CD36 is mainly expressed in tubular epithelial cells, podocytes and mesangial cells, and is markedly upregulated in the setting of chronic kidney disease (CKD). As fatty acids are the preferred energy source for proximal tubule cells, a reduction in fatty acid oxidation in CKD affects kidney lipid metabolism by disrupting the balance between fatty acid synthesis, uptake and consumption. The outcome is intracellular lipid accumulation, which has an important role in the pathogenesis of kidney fibrosis. In experimental models, antagonist blockade or genetic knockout of CD36 prevents kidney injury, suggesting that CD36 could be a novel target for therapy. Here, we discuss the regulation and post-translational modification of CD36, its role in renal pathophysiology and its potential as a biomarker and as a therapeutic target for the prevention of kidney fibrosis.

中文翻译：

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CD36在慢性肾脏疾病中的新见解和治疗机会

CD36（也称为清道夫受体B2）是一种多功能受体，可介导长链脂肪酸，氧化脂质和磷脂，高级氧化蛋白产物，血小板反应蛋白和高级糖基化终产物的结合和细胞摄取，并在脂质蓄积中起作用，发炎信号，能量重编程，细胞凋亡和肾纤维化。肾CD36主要在肾小管上皮细胞，足细胞和肾小球系膜细胞中表达，并在慢性肾脏疾病（CKD）的环境中显着上调。由于脂肪酸是近端小管细胞的首选能源，CKD中脂肪酸氧化的减少会破坏脂肪酸合成，摄取和消耗之间的平衡，从而影响肾脏的脂质代谢。结果是细胞内脂质积聚，在肾纤维化的发病机理中具有重要作用。在实验模型中，拮抗剂阻断或CD36的基因敲除可以防止肾脏损伤，这表明CD36可能是治疗的新靶标。在这里，我们讨论CD36的调节和翻译后修饰，其在肾脏病理生理中的作用以及其作为生物标志物和作为预防肾纤维化的治疗靶标的潜力。