TY - JOUR
T1 - Mitochondrial ROS deficiency and diabetic complications
T2 - AMP[K]-lifying the adaptation to hyperglycemia
AU - Towler, Dwight A.
PY - 2013/11/1
Y1 - 2013/11/1
N2 - Global, sustained production of ROS has deleterious effects on tissue structure and function and gives rise to biochemical and physiological changes associated with organ senescence. Specific, localized ROS metabolites generated by mitochondria and NADPH oxidases also transduce homeostatic information in response to metabolic, mechanical, and inflammatory cues. In this issue of the JCI, Dugan and colleagues demonstrate that mitochondrial-derived ROS, which is maintained by a feed-forward AMP kinase activation cascade, is reduced in diabetes and plays an adaptive role in preserving renal glomerular function during hyperglycemia. This enlightened view of mitochondrial ROS biology forces us to reconsider therapeutic approaches to metabolic disease complications such as diabetic nephropathy.
AB - Global, sustained production of ROS has deleterious effects on tissue structure and function and gives rise to biochemical and physiological changes associated with organ senescence. Specific, localized ROS metabolites generated by mitochondria and NADPH oxidases also transduce homeostatic information in response to metabolic, mechanical, and inflammatory cues. In this issue of the JCI, Dugan and colleagues demonstrate that mitochondrial-derived ROS, which is maintained by a feed-forward AMP kinase activation cascade, is reduced in diabetes and plays an adaptive role in preserving renal glomerular function during hyperglycemia. This enlightened view of mitochondrial ROS biology forces us to reconsider therapeutic approaches to metabolic disease complications such as diabetic nephropathy.
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U2 - 10.1172/JCI72326
DO - 10.1172/JCI72326
M3 - Article
C2 - 24135143
AN - SCOPUS:84887477574
SN - 0021-9738
VL - 123
SP - 4573
EP - 4576
JO - Journal of Clinical Investigation
JF - Journal of Clinical Investigation
IS - 11
ER -