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活性氧物种与线粒体自噬之间的分子调控机制及相互作用。

Molecular Regulation Mechanisms and Interactions Between Reactive Oxygen Species and Mitophagy.

机构信息

1 Department of Spine Center, Zhongda Hospital, Medical School, Southeast University , Nanjing, Jiangsu, China .

2 Department of Orthopaedic Surgery, Jiangyin Hospital of Traditional Chinese Medicine , Wuxi, Jiangsu, China .

出版信息

DNA Cell Biol. 2019 Jan;38(1):10-22. doi: 10.1089/dna.2018.4348. Epub 2018 Dec 15.

Abstract

The generation of reactive oxygen species (ROS) in response to oxidative stress has important effects on cell development, normal function, and survival. It may cause oxidative damage to intracellular macromolecular substances and mitochondria through several signaling pathways. However, the damaged mitochondria promote further ROS generation, creating a vicious cycle that can cause cellular injury. In addition, excessive ROS produced by damaged mitochondria can trigger mitophagy, a process that can scavenge impaired mitochondria and reduce ROS level to maintain stable mitochondrial function in cells. Therefore, mitophagy heaps maintain cellular homeostasis under oxidative stress. In this article, we review recent advances in cellular damage caused by excessive ROS, the mechanism of mitophagy, and the close relationship between ROS and mitophagy. This review provides a new perspective on therapeutic strategies for related diseases.

摘要

活性氧(ROS)的产生是细胞对氧化应激的一种反应,对细胞的发育、正常功能和存活有重要影响。ROS 可通过几种信号通路对细胞内的大分子物质和线粒体造成氧化损伤。然而,受损的线粒体促进进一步的 ROS 生成,形成一个恶性循环,从而导致细胞损伤。此外,受损线粒体产生的过多 ROS 可触发自噬,这一过程可以清除受损的线粒体,降低 ROS 水平,从而维持细胞中线粒体功能的稳定。因此,自噬可以在氧化应激下维持细胞内的稳态。本文综述了过量 ROS 引起的细胞损伤、自噬的机制以及 ROS 与自噬之间的密切关系。这一综述为相关疾病的治疗策略提供了新的视角。

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