Mechanism and Therapies of Oxidative Stress-Mediated Cell Death in Ischemia Reperfusion Injury

• Published in: Oxidative medicine and cellular longevity 2018-01, Vol.2018 (1), p.2910643-2910643
• Main Authors: Li, Haobo, Xia, Zhengyuan, Chen, Yanfang, Qi, Dake, Zheng, Hong
• Format: Article
• Language: English
• Subjects: Anesthesia; Animals; Antioxidants; Apoptosis; Cell Death; Drug dosages; Free radicals; Humans; Inflammation; Ischemia; Liver; Medicine; Oxidative Stress; Physiology; Reactive Oxygen Species - metabolism; Reperfusion Injury - metabolism; Reperfusion Injury - pathology; Reperfusion Injury - therapy; Rodents; Surgery
• ISSN: 1942-0900; 1942-0994
• DOI: 10.1155/2018/2910643

In this special issue, Z. Qiu et al. reported that, under hyperglycemic conditions, induction of nod-like receptor protein 3 (NLRP3) inflammasome-mediated pyroptotic cell death is critical in myocardial IRI, while inhibition of the inflammasome with specific inhibitors or ROS scavengers, N-acetylcysteine, reduced pyroptotic cell death and attenuated myocardial IRI. [...]oxidative stress-induced apoptotic and necroptotic cell deaths also play important roles in cardiac dysfunction as reported in this special issue by S. Peng et al. and N. Zeng et al, which showed that oxidative stress by increasing myocardial cell apoptosis and necroptosis leads to cardiac dysfunction in septic rats. Reperfusion-induced oxidative stress is the major contributor in IRI. [...]therapies that increase antioxidant capacity may protect organs against IRI [3]. Yan et al showed that treatment with PEP-1-heme oxgenase-1 fusion protein confers protection against septic shock-induced lung injury by reducing hepatic oxidative stress and inflammation, likely through suppression of toll-like receptor-4 and NF-κB. Aggravated inflammation, which has been shown to subsequently induce oxidative stress, has been proposed as a major cause of IRI and organ injury [8].