Targeting the Mitochondria in Heart Failure: A Translational Perspective.

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ID: 96359
2020
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Abstract
The burden of heart failure (HF) in terms of health care expenditures, hospitalizations, and mortality is substantial and growing. The failing heart has been described as "energy-deprived" and mitochondrial dysfunction is a driving force associated with this energy supply-demand imbalance. Existing HF therapies provide symptomatic and longevity benefit by reducing cardiac workload through heart rate reduction and reduction of preload and afterload but do not address the underlying causes of abnormal myocardial energetic nor directly target mitochondrial abnormalities. Numerous studies in animal models of HF as well as myocardial tissue from explanted failed human hearts have shown that the failing heart manifests abnormalities of mitochondrial structure, dynamics, and function that lead to a marked increase in the formation of damaging reactive oxygen species and a marked reduction in on demand adenosine triphosphate synthesis. Correcting mitochondrial dysfunction therefore offers considerable potential as a new therapeutic approach to improve overall cardiac function, quality of life, and survival for patients with HF.
Reference Key
sabbah2020targetingjacc Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Sabbah, Hani N;
Journal jacc basic to translational science
Year 2020
DOI
10.1016/j.jacbts.2019.07.009
URL
Keywords
mitochondria heart failure oxidative phosphorylation cardiolipin ros, reactive oxygen species hf, heart failure adp, adenosine diphosphate atp, adenosine triphosphate ci (to v), complex i (to v) drp, dynamin-related protein etc, electron transport chain hfpef, heart failure with preserved ejection fraction hfref, heart failure with reduced ejection fraction lv, left ventricular mptp, mitochondrial permeability transition pore mfn, mitofusin opa, optic atrophy pgc, peroxisome proliferator-activated receptor coactivator pink, phosphatase and tensin homolog–inducible kinase taz, tafazzin mtdna, mitochondrial deoxyribonucleic acid myocardial energetics

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