Mitochondrial ROS deficiency and diabetic complications

AMP[K]-lifying the adaptation to hyperglycemia

Research output: Contribution to journalArticle

14 Citations (Scopus)

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

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Adenylate Kinase
NADPH Oxidase
Metabolic Diseases
Diabetic Nephropathies
Diabetes Complications
Adenosine Monophosphate
Hyperglycemia
Cues
Mitochondria
Kidney
Therapeutics

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Mitochondrial ROS deficiency and diabetic complications : AMP[K]-lifying the adaptation to hyperglycemia. / Towler, Dwight A.

In: Journal of Clinical Investigation, Vol. 123, No. 11, 01.11.2013, p. 4573-4576.

Research output: Contribution to journalArticle

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