Oxidative stress and autophagy: crucial modulators of kidney injury.
Oxidative stress and autophagy: crucial modulators of kidney injury.
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DOI：
10.1016/j.redox.2015.01.001
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发表时间：
2015
期刊：
影响因子：
11.4
通讯作者：
Choi ME
中科院分区：
文献类型：
--
作者：
Sureshbabu A;Ryter SW;Choi ME
导致肾功能下降的急性肾损伤（AKI）和慢性肾脏病（CKD）都是死亡率增加的相互依赖的风险因素。如果长期不治疗，终末期肾病（ESRD）是不可避免的结果。急慢性肾脏疾病的发生部分是由于调控氧化应激、炎症、自噬和细胞死亡的分子机制之间的失衡。氧化应激是指引起细胞损伤的高活性氧化分子的累积效应。自噬通过将受损的细胞器、蛋白质聚集体和病原体招募到称为自噬体的双层膜囊泡中，随后自噬体与溶酶体融合，从而清除这些物质。越来越多的证据表明，氧化应激和自噬都显著参与肾脏健康和疾病。然而，对于连接它们的信号传导过程知之甚少。本综述着重于理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可能存在的关系，这些关系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。
氧化应激反应调节和自噬的潜在分子机制可能存在大量的相互作用。
自噬途径可能在肾脏疾病的背景下受到调控。自噬途径的失效或中断可能导致肾脏疾病的发病机制。
针对自噬途径在肾脏疾病的治疗和管理中可能具有相当大的治疗潜力。
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. The molecular mechanisms underlying the regulation of oxidative stress responses and autophagy may exhibit considerable cross-talk. The autophagy pathway may be regulated in the context of kidney diseases. Failure or disruption of the autophagy pathway may contribute to the pathogenesis of kidney diseases. Targeting the autophagy pathway may show considerable therapeutic potential in the treatment and management of kidney disorders.