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ROS 调控的自噬作用:生理与病理。

Regulation of autophagy by ROS: physiology and pathology.

机构信息

Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, 76100, Israel.

出版信息

Trends Biochem Sci. 2011 Jan;36(1):30-8. doi: 10.1016/j.tibs.2010.07.007. Epub 2010 Aug 20.

Abstract

Reactive oxygen species (ROS) are small and highly reactive molecules that can oxidize proteins, lipids and DNA. When tightly controlled, ROS serve as signaling molecules by modulating the activity of the oxidized targets. Accumulating data point to an essential role for ROS in the activation of autophagy. Be the outcome of autophagy survival or death and the initiation conditions starvation, pathogens or death receptors, ROS are invariably involved. The nature of this involvement, however, remains unclear. Moreover, although connections between ROS and autophagy are observed in diverse pathological conditions, the mode of activation of autophagy and its potential protective role remain incompletely understood. Notably, recent advances in the field of redox regulation of autophagy focus on the role of mitochondria as a source of ROS and on mitophagy as a means for clearance of ROS.

摘要

活性氧(ROS)是体积小、反应活性高的分子,可以氧化蛋白质、脂质和 DNA。当受到严格控制时,ROS 通过调节氧化靶标活性充当信号分子。越来越多的数据表明 ROS 在自噬的激活中起重要作用。无论是自噬的结果是生存还是死亡,以及起始条件是饥饿、病原体还是死亡受体,ROS 都始终参与其中。然而,这种参与的性质尚不清楚。此外,尽管在各种病理条件下都观察到了 ROS 和自噬之间的联系,但自噬的激活方式及其潜在的保护作用仍不完全清楚。值得注意的是,自噬的氧化还原调节领域的最新进展侧重于线粒体作为 ROS 来源的作用以及作为清除 ROS 的手段的线粒体自噬。

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