Kong Weiwei, Liao Yixin, Zhao Liang, Hall Nathan, Zhou Hua, Liu Ruisheng, Persson Pontus B, Lai Enyin
Kidney Disease Center of First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Department of Physiology, School of Basic Medical Sciences, Zhejiang University School of Medicine, Hangzhou 310003, China.
Biomedicines. 2023 Nov 6;11(11):2984. doi: 10.3390/biomedicines11112984.
The renin-angiotensin system (RAS) and hypoxia have a complex interaction: RAS is activated under hypoxia and activated RAS aggravates hypoxia in reverse. Renin is an aspartyl protease that catalyzes the first step of RAS and tightly regulates RAS activation. Here, we outline kidney renin expression and release under hypoxia and discuss the putative mechanisms involved. It is important that renin generally increases in response to acute hypoxemic hypoxia and intermittent hypoxemic hypoxia, but not under chronic hypoxemic hypoxia. The increase in renin activity can also be observed in anemic hypoxia and carbon monoxide-induced histotoxic hypoxia. The increased renin is contributed to by juxtaglomerular cells and the recruitment of renin lineage cells. Potential mechanisms regulating hypoxic renin expression involve hypoxia-inducible factor signaling, natriuretic peptides, nitric oxide, and Notch signaling-induced renin transcription.
肾素-血管紧张素系统(RAS)与缺氧存在复杂的相互作用:缺氧时RAS被激活,而激活的RAS又会反过来加重缺氧。肾素是一种天冬氨酰蛋白酶,它催化RAS的第一步反应,并严格调控RAS的激活。在此,我们概述了缺氧条件下肾脏肾素的表达与释放,并讨论其中涉及的可能机制。重要的是,肾素通常会对急性低氧性缺氧和间歇性低氧性缺氧产生反应而增加,但在慢性低氧性缺氧条件下则不会。在贫血性缺氧和一氧化碳诱导的组织中毒性缺氧中也可观察到肾素活性增加。肾素增加是由肾小球旁细胞和肾素谱系细胞的募集所致。调节缺氧性肾素表达的潜在机制包括缺氧诱导因子信号传导、利钠肽、一氧化氮以及Notch信号诱导的肾素转录。