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- W3007510132 endingPage "33" @default.
- W3007510132 startingPage "33" @default.
- W3007510132 abstract "Mitochondrial medicine is increasingly discussed as a promising therapeutic approach, given that mitochondrial defects are thought to contribute to many prevalent diseases and their complications. In individuals with diabetes mellitus (DM), defects in mitochondrial structure and function occur in many organs throughout the body, contributing both to the pathogenesis of DM and complications of DM. Diabetic cardiomyopathy (DbCM) is increasingly recognized as an underlying cause of increased heart failure in DM, and several mitochondrial mechanisms have been proposed to contribute to the development of DbCM. Well established mechanisms include myocardial energy depletion due to impaired adenosine triphosphate (ATP) synthesis and mitochondrial uncoupling, and increased mitochondrial oxidative stress. A variety of upstream mechanisms of impaired ATP regeneration and increased mitochondrial reactive oxygen species have been proposed, and recent studies now also suggest alterations in mitochondrial dynamics and autophagy, impaired mitochondrial Ca²⁺ uptake, decreased cardiac adiponectin action, increased O-GlcNAcylation, and impaired activity of sirtuins to contribute to mitochondrial defects in DbCM, among others. In the current review, we present and discuss the evidence that underlies both established and recently proposed mechanisms that are thought to contribute to mitochondrial dysfunction in DbCM." @default.
- W3007510132 created "2020-03-06" @default.
- W3007510132 creator A5021427999 @default.
- W3007510132 creator A5038456704 @default.
- W3007510132 creator A5090858003 @default.
- W3007510132 date "2020-01-01" @default.
- W3007510132 modified "2023-10-02" @default.
- W3007510132 title "Mitochondrial Mechanisms in Diabetic Cardiomyopathy" @default.
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