Mitochondrial reactive oxygen species in the pathogenesis of early diabetic nephropathy

Takeshi Nishikawa; Michael Brownlee; Eiichi Araki

doi:10.1111/jdi.12258

Mitochondrial reactive oxygen species in the pathogenesis of early diabetic nephropathy

Takeshi Nishikawa, Michael Brownlee, Eiichi Araki

Medicine

Research output: Contribution to journal › Article › peer-review

40 Scopus citations

Abstract

Dugan et al. reported model of a feed-forward cycle involving decreased AMPK activity and decreased mitochondrial biogenesis caused by decreased ROS as a proposed mechanism involved in the pathogenesis of diabetic nephropathy. However, in this commentary, we proposed an alternate model of a feed-forward cycle involving decreased AMPK activity and decreased mitochondrial biogenesis caused by increased mitochondrial ROS.

Original language	English (US)
Pages (from-to)	137-139
Number of pages	3
Journal	Journal of Diabetes Investigation
Volume	6
Issue number	2
DOIs	https://doi.org/10.1111/jdi.12258
State	Published - Mar 1 2015

ASJC Scopus subject areas

Internal Medicine
Endocrinology, Diabetes and Metabolism

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1111/jdi.12258

Cite this

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abstract = "Dugan et al. reported model of a feed-forward cycle involving decreased AMPK activity and decreased mitochondrial biogenesis caused by decreased ROS as a proposed mechanism involved in the pathogenesis of diabetic nephropathy. However, in this commentary, we proposed an alternate model of a feed-forward cycle involving decreased AMPK activity and decreased mitochondrial biogenesis caused by increased mitochondrial ROS.",

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Mitochondrial reactive oxygen species in the pathogenesis of early diabetic nephropathy

Abstract

ASJC Scopus subject areas

UN SDGs

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