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Oxidative Medicine and Cellular Longevity
Volume 2016 (2016), Article ID 4350965, 18 pages
http://dx.doi.org/10.1155/2016/4350965
Review Article

ROS and ROS-Mediated Cellular Signaling

1Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
2Department of Plastic Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China
3Department of Hospital Infection Office, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China

Received 10 August 2015; Revised 1 December 2015; Accepted 20 December 2015

Academic Editor: Javier Egea

Copyright © 2016 Jixiang Zhang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

It has long been recognized that an increase of reactive oxygen species (ROS) can modify the cell-signaling proteins and have functional consequences, which successively mediate pathological processes such as atherosclerosis, diabetes, unchecked growth, neurodegeneration, inflammation, and aging. While numerous articles have demonstrated the impacts of ROS on various signaling pathways and clarify the mechanism of action of cell-signaling proteins, their influence on the level of intracellular ROS, and their complex interactions among multiple ROS associated signaling pathways, the systemic summary is necessary. In this review paper, we particularly focus on the pattern of the generation and homeostasis of intracellular ROS, the mechanisms and targets of ROS impacting on cell-signaling proteins (NF-κB, MAPKs, Keap1-Nrf2-ARE, and PI3K-Akt), ion channels and transporters (Ca2+ and mPTP), and modifying protein kinase and Ubiquitination/Proteasome System.