Deconvoluting the role of reactive oxygen species and autophagy in human diseases.

Xin Wen, Jinming Wu, Fengtian Wang, Bo Liu, Canhua Huang, Yuquan Wei

Journal: Free radical biology & medicine 2015;65():402-410

PMID: 23872397

Full Text on Elsevier Science View on PubMed

Abstract

Reactive oxygen species (ROS), chemically reactive molecules containing oxygen, can form as a natural byproduct of the normal metabolism of oxygen and also have their crucial roles in cell homeostasis. Of note, the major intracellular sources including mitochondria, endoplasmic reticulum (ER), peroxisomes and the NADPH oxidase (NOX) complex have been identified in cell membranes to produce ROS. Interestingly, autophagy, an evolutionarily conserved lysosomal degradation process in which a cell degrades long-lived proteins and damaged organelles, has recently been well-characterized to be regulated by different types of ROS. Accumulating evidence has demonstrated that ROS-modulated autophagy has numerous links to a number of pathological processes, including cancer, ageing, neurodegenerative diseases, type-II diabetes, cardiovascular diseases, muscular disorders, hepatic encephalopathy and immunity diseases. In this review, we focus on summarizing the molecular mechanisms of ROS-regulated autophagy and their relevance to diverse diseases, which would shed new light on more ROS modulators as potential therapeutic drugs for fighting human diseases.

Address: State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China.; College of Life Sciences, Sichuan University, Chengdu 610064, China.; State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China. Electronic address: [email protected].; State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu 610041, China. Electronic address: [email protected].

DOI: 10.1016/j.freeradbiomed.2013.07.013