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Journal of Diabetes Research
Volume 2017, Article ID 4826724, 15 pages
Review Article

The Nrf2/Keap1/ARE Pathway and Oxidative Stress as a Therapeutic Target in Type II Diabetes Mellitus

Hansjörg Wyss Department of Plastic and Reconstructive Surgery, New York University School of Medicine, 430 East 29th Street, New York, NY 10016, USA

Correspondence should be addressed to Daniel J. Ceradini; gro.cmuyn@inidarec.leinad

Received 12 April 2017; Revised 3 July 2017; Accepted 20 July 2017; Published 20 August 2017

Academic Editor: Joseph F. Ndisang

Copyright © 2017 Joshua A. David et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Despite improvements in awareness and treatment of type II diabetes mellitus (TIIDM), this disease remains a major source of morbidity and mortality worldwide, and prevalence continues to rise. Oxidative damage caused by free radicals has long been known to contribute to the pathogenesis and progression of TIIDM and its complications. Only recently, however, has the role of the Nrf2/Keap1/ARE master antioxidant pathway in diabetic dysfunction begun to be elucidated. There is accumulating evidence that this pathway is implicated in diabetic damage to the pancreas, heart, and skin, among other cell types and tissues. Animal studies and clinical trials have shown promising results suggesting that activation of this pathway can delay or reverse some of these impairments in TIIDM. In this review, we outline the role of oxidative damage and the Nrf2/Keap1/ARE pathway in TIIDM, focusing on current and future efforts to utilize this relationship as a therapeutic target for prevention, prognosis, and treatment of TIID.