Pro-renin receptor suppresses mitochondrial biogenesis and function via AMPK/SIRT-1/PGC-1α pathway in diabetic kidney
Pro-renin receptor suppresses mitochondrial biogenesis and function via AMPK/SIRT-1/PGC-1α pathway in diabetic kidney
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DOI：
10.1371/journal.pone.0225728
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发表时间：
2019-12-04
期刊：
影响因子：
3.7
通讯作者：
Siragy, Helmy M.
中科院分区：
文献类型：
--
作者：
Akhtar, Safia;Siragy, Helmy M.
线粒体的生物发生和功能异常与包括糖尿病在内的多种疾病有关。最近，我们证实了肾(Pro)肾素受体(PRR)在线粒体失调中的作用。我们推测PRR通过PGC-1α/AMPK/SIRT-1信号通路参与糖尿病大鼠肾脏线粒体生物合成和功能的降低。用C57BL/6小鼠和小鼠肾小球系膜细胞(MRMCs)进行体内和体外研究。对照组和链脲佐菌素诱导的糖尿病小鼠注射scurble或PrR shRNA，并跟踪观察8周。PRR基因和蛋白表达分别增加44%和39%(P
Abnormal mitochondrial biogenesis and function has been linked to multiple diseases including diabetes. Recently, we demonstrated the role of renal (Pro)renin receptor (PRR) in the dysregulation of mitochondria. We hypothesized that PRR contributes to the reduction of mitochondrial biogenesis and function in diabetic kidney via PGC-1 alpha/AMPK/SIRT-1 signaling pathway. In vivo and in vitro studies were conducted in C57BL/6 mouse and mouse renal mesangial cells (mRMCs). Control and streptozotocin-induced diabetic mice were injected with scramble or PRR shRNA and followed for a period of eight weeks. PRR mRNA and protein expression increased by 44% and 39% respectively (P