title: Cardiac metabolism in heart failure: implications beyond ATP production.
abstract: The heart has a high rate of ATP production and turnover that is required to maintain its continuous mechanical work. Perturbations in ATP-generating processes may therefore affect contractile function directly. Characterizing cardiac metabolism in heart failure (HF) revealed several metabolic alterations called metabolic remodeling, ranging from changes in substrate use to mitochondrial dysfunction, ultimately resulting in ATP deficiency and impaired contractility. However, ATP depletion is not the only relevant consequence of metabolic remodeling during HF. By providing cellular building blocks and signaling molecules, metabolic pathways control essential processes such as cell growth and regeneration. Thus, alterations in cardiac metabolism may also affect the progression to HF by mechanisms beyond ATP supply. Our aim is therefore to highlight that metabolic remodeling in HF not only results in impaired cardiac energetics but also induces other processes implicated in the development of HF such as structural remodeling and oxidative stress. Accordingly, modulating cardiac metabolism in HF may have significant therapeutic relevance that goes beyond the energetic aspect.
authors.affiliation: Department of Cardiothoracic Surgery, Jena University Hospital, Friedrich-Schiller-University Jena, Germany. doenst@med.uni-jena.de
authors.forename: Torsten
authors.initials: T
authors.lastname: Doenst
authors.forename: Tien Dung
authors.initials: TD
authors.lastname: Nguyen
authors.forename: E Dale
authors.initials: ED
authors.lastname: Abel
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis*; D000818:Animals; D004734:Energy Metabolism; D005947:Glucose / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*
chemical_list: D000255:Adenosine Triphosphate; D005947:Glucose
keywords: heart failure; hypertrophy/remodeling; metabolism; mitochondria