Oxidative Stress and Inflammation Interaction in Ischemia Reperfusion Injury: Role of Programmed Cell Death

Zheng et al. demonstrated that the induction of pyroptotic cell death mediated via nod-like receptor protein-3 (NLRP3) inflammasome is critical in high-fat diet-induced kidney damage and that the downregulation of vascular endothelial growth factor receptor-2 (VEGFR2) not only reduced NLRP3 activati...

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Published in:Oxidative medicine and cellular longevity 2019-01, Vol.2019, p.6780816-2
Main Authors: Yao, Weifeng, Tai, Lydia Wai, Liu, Yiwei, Hei, Ziqing, Li, Haobo
Format: Article
Language:English
Subjects:
Animals
Antioxidants
Apoptosis
Autophagy
Biochemistry
Cell Death
Diabetes
Editorials
Free radicals
Humans
Inflammation
Inflammation - genetics
Ischemia
Kidneys
Liver
Liver diseases
Medicine
Mice
Oxidases
Oxidation
Oxidative Stress
Physiology
Reperfusion Injury
Rodents
Roles
Stem cells
Transplantation of organs, tissues, etc
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Summary:Zheng et al. demonstrated that the induction of pyroptotic cell death mediated via nod-like receptor protein-3 (NLRP3) inflammasome is critical in high-fat diet-induced kidney damage and that the downregulation of vascular endothelial growth factor receptor-2 (VEGFR2) not only reduced NLRP3 activation but also attenuated kidney injury in high-fat diet-treated mice. [...]Y. Wang et al. reported that in mouse transient global cerebral ischemia (TGCI), decreased autophagy was accompanied by increased apoptosis in neurons that were associated with neurological dysfunction. The importance of oxidative stress in the cause of IRI has been well recognized [4]. [...]therapies that reduce oxidative stress either by increasing antioxidant capacity or by decreasing ROS production may protect organs against IRI. [...]in-depth studies regarding the interaction of inflammation and oxidative stress in the setting of IRI may facilitate our understanding of the pathophysiology of IRI and the development of new therapies for the disease.
ISSN:1942-0900
1942-0994
DOI:10.1155/2019/6780816