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- W2964282047 endingPage "3552" @default.
- W2964282047 startingPage "3552" @default.
- W2964282047 abstract "Heart failure (HF) frequently coexists with conditions associated with glucose insufficiency, such as insulin resistance and type 2 diabetes mellitus (T2DM), and patients with T2DM have a significantly high incidence of HF. These two closely related diseases cannot be separated on the basis of their treatment. Some antidiabetic drugs failed to improve cardiac outcomes in T2DM patients, despite lowering glucose levels sufficiently. This may be, at least in part, due to a lack of understanding of cardiac insulin resistance. Basic investigations have revealed the significant contribution of cardiac insulin resistance to the pathogenesis and progression of HF; however, there is no clinical evidence of the definition or treatment of cardiac insulin resistance. Mitochondrial dynamics play an important role in cardiac insulin resistance and HF because they maintain cellular homeostasis through energy production, cell survival, and cell proliferation. The innovation of diagnostic tools and/or treatment targeting mitochondrial dynamics is assumed to improve not only the insulin sensitivity of the myocardium and cardiac metabolism, but also the cardiac contraction function. In this review, we summarized the current knowledge on the correlation between cardiac insulin resistance and progression of HF, and discussed the role of mitochondrial dynamics on the pathogenesis of cardiac insulin resistance and HF. We further discuss the possibility of mitochondria-targeted intervention to improve cardiac metabolism and HF." @default.
- W2964282047 created "2019-07-30" @default.
- W2964282047 creator A5016609222 @default.
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- W2964282047 creator A5065273201 @default.
- W2964282047 creator A5088202260 @default.
- W2964282047 date "2019-07-20" @default.
- W2964282047 modified "2023-10-14" @default.
- W2964282047 title "Cardiac Insulin Resistance in Heart Failure: The Role of Mitochondrial Dynamics" @default.
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- W2964282047 doi "https://doi.org/10.3390/ijms20143552" @default.
- W2964282047 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6678249" @default.
- W2964282047 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31330848" @default.
- W2964282047 hasPublicationYear "2019" @default.
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