Mitochondrial ROS deficiency and diabetic complications: AMP[K]-lifying the adaptation to hyperglycemia

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16 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4573-4576
Number of pages4
JournalJournal of Clinical Investigation
Volume123
Issue number11
DOIs
StatePublished - Nov 1 2013

ASJC Scopus subject areas

  • Medicine(all)

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