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2017 ; 2017
(ä): 4826724
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The Nrf2/Keap1/ARE Pathway and Oxidative Stress as a Therapeutic Target in Type
II Diabetes Mellitus
#MMPMID28913364
David JA
; Rifkin WJ
; Rabbani PS
; Ceradini DJ
J Diabetes Res
2017[]; 2017
(ä): 4826724
PMID28913364
show ga
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.
|Carboxylic Ester Hydrolases/*metabolism
[MESH]
|Diabetes Mellitus, Type 2/*drug therapy/metabolism
[MESH]
|Humans
[MESH]
|Hypoglycemic Agents/pharmacology/*therapeutic use
[MESH]
|Kelch-Like ECH-Associated Protein 1/*metabolism
[MESH]