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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 6437467, 12 pages
https://doi.org/10.1155/2017/6437467
Review Article

Insights for Oxidative Stress and mTOR Signaling in Myocardial Ischemia/Reperfusion Injury under Diabetes

1Department of Cardiac Surgery, Xijing Hospital, The Fourth Military Medical University, Xi’an 710032, China
2Department of Anesthesiology, Xi’an Children’s Hospital, Xi’an 710003, China

Correspondence should be addressed to Jian Yang; nc.ude.ummf@naijgnay and Lifang Yang; moc.liamtoh@6gnafilgnay

Received 8 September 2016; Revised 1 December 2016; Accepted 4 January 2017; Published 19 February 2017

Academic Editor: Flávio Reis

Copyright © 2017 Dajun Zhao 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

Diabetes mellitus (DM) displays a high morbidity. The diabetic heart is susceptible to myocardial ischemia/reperfusion (MI/R) injury. Impaired activation of prosurvival pathways, endoplasmic reticulum (ER) stress, increased basal oxidative state, and decreased antioxidant defense and autophagy may render diabetic hearts more vulnerable to MI/R injury. Oxidative stress and mTOR signaling crucially regulate cardiometabolism, affecting MI/R injury under diabetes. Producing reactive oxygen species (ROS) and reactive nitrogen species (RNS), uncoupling nitric oxide synthase (NOS), and disturbing the mitochondrial quality control may be three major mechanisms of oxidative stress. mTOR signaling presents both cardioprotective and cardiotoxic effects on the diabetic heart, which interplays with oxidative stress directly or indirectly. Antihyperglycemic agent metformin and newly found free radicals scavengers, Sirt1 and CTRP9, may serve as promising pharmacological therapeutic targets. In this review, we will focus on the role of oxidative stress and mTOR signaling in the pathophysiology of MI/R injury in diabetes and discuss potential mechanisms and their interactions in an effort to provide some evidence for cardiometabolic targeted therapies for ischemic heart disease (IHD).