Activation of TRPV1 channel antagonizes diabetic nephropathy through inhibiting endoplasmic reticulum-mitochondria contact in podocytes

The impairment of podocyte protein filtration function caused by excessive mitochondrial calcium intake is a critical feature of diabetic nephropathy (DN). Ca2+ channel transient receptor potential cation channel subfamily V member 1 (TRPV1) has been reported to protect against ischemia-reperfusion induced acute renal injury, but there is no report about its role in DN. Here, we report that dietary capsaicin potently inhibits and reverses chronic renal structural and functional damages in db/db or streptozotocin (STZ)-induced diabetic mice in a TRPV1-dependent manner.

Source: Metabolism - Clinical and Experimental - February 13, 2020 Category: Biomedical Science Authors: Xiao Wei, Xing Wei, ZongShi Lu, Li Li, YingRu Hu, Fang Sun, YanLi Jiang, Huan Ma, HongTing Zheng, GangYi Yang, DaoYan Liu, Peng Gao, ZhiMing Zhu Source Type: research