Sureshbabu Angara, Ryter Stefan W, Choi Mary E
Joan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, Weill Cornell Medical College, New York, NY, USA.
Joan and Sanford I. Weill Department of Medicine, New York-Presbyterian Hospital, Weill Cornell Medical College, New York, NY, USA.
Redox Biol. 2015;4:208-14. doi: 10.1016/j.redox.2015.01.001. Epub 2015 Jan 13.
Both acute kidney injury (AKI) and chronic kidney disease (CKD) that lead to diminished kidney function are interdependent risk factors for increased mortality. If untreated over time, end stage renal disease (ESRD) is an inevitable outcome. Acute and chronic kidney diseases occur partly due to imbalance between the molecular mechanisms that govern oxidative stress, inflammation, autophagy and cell death. Oxidative stress refers to the cumulative effects of highly reactive oxidizing molecules that cause cellular damage. Autophagy removes damaged organelles, protein aggregates and pathogens by recruiting these substrates into double membrane vesicles called autophagosomes which subsequently fuse with lysosomes. Mounting evidence suggests that both oxidative stress and autophagy are significantly involved in kidney health and disease. However, very little is known about the signaling processes that link them. This review is focused on understanding the role of oxidative stress and autophagy in kidney diseases. In this review, we also discuss the potential relationships between oxidative stress and autophagy that may enable the development of better therapeutic intervention to halt the progression of kidney disease and promote its repair and resolution.
导致肾功能减退的急性肾损伤(AKI)和慢性肾脏病(CKD)都是死亡率增加的相互依存的危险因素。如果长期不治疗,终末期肾病(ESRD)是不可避免的结果。急性和慢性肾脏病的发生部分是由于控制氧化应激、炎症、自噬和细胞死亡的分子机制之间的失衡。氧化应激是指高反应性氧化分子导致细胞损伤的累积效应。自噬通过将这些底物招募到称为自噬体的双膜囊泡中来清除受损的细胞器、蛋白质聚集体和病原体,这些自噬体随后与溶酶体融合。越来越多的证据表明,氧化应激和自噬都与肾脏健康和疾病密切相关。然而,关于连接它们的信号传导过程却知之甚少。本综述着重于了解氧化应激和自噬在肾脏疾病中的作用。在本综述中,我们还讨论了氧化应激和自噬之间的潜在关系,这可能有助于开发更好的治疗干预措施,以阻止肾脏疾病的进展并促进其修复和缓解。