Cellular metabolic and autophagic pathways: Traffic control by redox signaling

被引:268
|
作者
Dodson, Matthew [1 ,2 ,3 ]
Darley-Usmar, Victor [1 ,2 ,3 ]
Zhang, Jianhua [1 ,2 ,3 ,4 ]
机构
[1] Ctr Free Rad Biol, Birmingham, AL 35294 USA
[2] Univ Alabama Birmingham, Birmingham, AL 35294 USA
[3] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL 35294 USA
[4] Birmingham VA Med Ctr, Dept Vet Affairs, Birmingham, AL 35233 USA
关键词
Autophagy; Mitophagy; Oxidative stress; Redox signaling; Cellular bioenergetics; Mitochondria; Glucose; Glycolysis; Glutathione; Aging; Cardiovascular disease; Neurodegeneration; Diabetes; Free radicals; ELECTRON-TRANSPORT-CHAIN; NEGATIVELY REGULATES AUTOPHAGY; CHAPERONE-MEDIATED AUTOPHAGY; ENDOPLASMIC-RETICULUM STRESS; PENTOSE-PHOSPHATE PATHWAY; OXIDATIVE STRESS; LIPID-PEROXIDATION; NITRIC-OXIDE; MITOCHONDRIAL DYSFUNCTION; GLUCOSE-METABOLISM;
D O I
10.1016/j.freeradbiomed.2013.05.014
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
It has been established that the key metabolic pathways of glycolysis and oxidative phosphorylation are intimately related to redox biology through control of cell signaling. Under physiological conditions glucose metabolism is linked to control of the NADH/NAD redox couple, as well as providing the major reductant, NADPH, for thiol-dependent antioxidant defenses. Retrograde signaling from the mitochondrion to the nucleus or cytosol controls cell growth and differentiation. Under pathological conditions mitochondria are targets for reactive oxygen and nitrogen species and are critical in controlling apoptotic cell death. At the interface of these metabolic pathways, the autophagy-lysosomal pathway functions to maintain mitochondrial quality and generally serves an important cytoprotective function. In this review we will discuss the autophagic response to reactive oxygen and nitrogen species that are generated from perturbations of cellular glucose metabolism and bioenergetic function. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:207 / 221
页数:15
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