Glycoxidative stress-induced mitophagy modulates mitochondrial fates

Annals of the New York Academy of Sciences
Mei-Chen LoShu-Huei Kao

Abstract

Diabetes mellitus (DM), a state of chronic hyperglycemia, is associated with a variety of serious complications. Hyperglycemia-induced advanced glycation end products (AGEs) play an important role in the development of diabetic complications. In vivo, we demonstrated that disrupted mitochondria and autophagy was elevated in type II DM db/db mice. Mitophagy was evidenced by increased autophagosome formation in the beta-islet cells. The adducts of N(epsilon)-(carboxymethyl) lysine (CML), a major AGE, and bovine serum albumin (CML-BSA) stimulated the conversion of microtubule-associated protein 1 light chain 3-I (LC3-I) to LC3-II in rat insulinoma cells (RIN-m5F). CML-BSA increased ROS generation as demonstrated in a time-dependent manner. Experiments with mitochondrial targeted enhanced yellow fluorescent protein transfected RIN-m5F cells, massive fragmented mitochondria were visualized in the CML-BSA treated cells. Taken together, these data suggested that AGEs may cause mitochondrial dysfunction and mitophagosome formation, and AGEs-induced glycoxidative stress may trigger mitophagic process to modulate mitochondrial fates leading to either cell survival or cell death.

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Citations

Feb 4, 2012·ASN Neuro·Shinichi TakahashiNorihiro Suzuki
Jul 11, 2012·International Journal of Cell Biology·Pamela Boon Li Pun, Michael P Murphy
Jan 21, 2012·Rinshō shinkeigaku = Clinical neurology·Shinichi TakahashiNorihiro Suzuki
Apr 17, 2012·Journal of Smooth Muscle Research = Nihon Heikatsukin Gakkai Kikanshi·Meenal Pangare, Ayako Makino
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Jun 20, 2017·Oxidative Medicine and Cellular Longevity·Sijie Tan, Esther Wong
Apr 12, 2014·Hormones : International Journal of Endocrinology and Metabolism·Evangelia TantalakiEvanthia Diamanti-Kandarakis

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