Zhou Xun, Chen Hui, Shi Yingfeng, Ma Xiaoyan, Zhuang Shougang, Liu Na
Department of Nephrology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Department of Medicine, Rhode Island Hospital and Alpert Medical School, Brown University, Providence, RI, United States.
Front Pharmacol. 2021 Jun 16;12:695237. doi: 10.3389/fphar.2021.695237. eCollection 2021.
Acute kidney injury (AKI) is a common clinical complication with an incidence of up to 8-18% in hospitalized patients. AKI is also a complication of COVID-19 patients and is associated with an increased risk of death. In recent years, numerous studies have suggested that epigenetic regulation is critically involved in the pathophysiological process and prognosis of AKI. Histone acetylation, one of the epigenetic regulations, is negatively regulated by histone deacetylases (HDACs). Increasing evidence indicates that HDACs play an important role in the pathophysiological development of AKI by regulation of apoptosis, inflammation, oxidative stress, fibrosis, cell survival, autophagy, ATP production, and mitochondrial biogenesis (MB). In this review, we summarize and discuss the role and mechanism of HDACs in the pathogenesis of AKI.
急性肾损伤（AKI）是一种常见的临床并发症，在住院患者中的发病率高达8%-18%。AKI也是新型冠状病毒肺炎（COVID-19）患者的并发症，且与死亡风险增加相关。近年来，大量研究表明，表观遗传调控在AKI的病理生理过程和预后中起关键作用。组蛋白乙酰化作为表观遗传调控之一，受组蛋白去乙酰化酶（HDACs）负调控。越来越多的证据表明，HDACs通过调节细胞凋亡、炎症、氧化应激、纤维化、细胞存活、自噬、ATP生成和线粒体生物合成（MB），在AKI的病理生理发展中起重要作用。在本综述中，我们总结并讨论了HDACs在AKI发病机制中的作用和机制。
