Role of intracellular renin and (pro)renin receptor in cardiac myocytes

在本研究中，我们发现糖尿病心脏缺血时细胞内肾素在细胞质和线粒体中的表达增加，并且肾素的增加可以保护心肌细胞免受缺血损伤。肾素的这种保护作用是由于UCP的减少和电子传递链的加速，从而在缺血应激下阻止线粒体去极化和维持ATP的产生。肾素的心脏保护作用独立于随后的细胞内血管紧张素II的产生。这些结果表明，与先前报道的循环RAS的不良作用相反，胞质肾素在糖尿病心脏中保护心肌细胞免受缺血应激的重要作用。

In this study, we found that expression of intracellular renin increased both in cytosol and mitochondriaduring ischemia in diabetic heart, and that increased renin protects cardiomyocytes from ischemic injury. This protective effect of renin is due to the reduction of UCP and acceleration of electron transport chain, which resulted in the prevention of mitochondrial depolarization and preservation of ATP production under ischemic stress. The cardioprotective effect of renin is independent from subsequent intracellular angiotensin II production.These results indicated that in contrast to previously reported adverse effects of circulating RAS, cytosolic renin plays an important role to protect myocytes from ischemic stress in diabetic heart.