title: Mitochondria as a therapeutic target in heart failure.
abstract: Heart failure is a pressing public health problem with no curative treatment currently available. The existing therapies provide symptomatic relief, but are unable to reverse molecular changes that occur in cardiomyocytes. The mechanisms of heart failure are complex and multiple, but mitochondrial dysfunction appears to be a critical factor in the development of this disease. Thus, it is important to focus research efforts on targeting mitochondrial dysfunction in the failing heart to revive the myocardium and its contractile function. This review highlights the 3 promising areas for the development of heart failure therapies, including mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial iron handling. Moreover, the translational potential of compounds targeting these pathways is discussed.
authors.affiliation: Feinberg Cardiovascular Research Institute, Northwestern University School of Medicine, Chicago, Illinois, USA.
authors.forename: Marina
authors.initials: M
authors.lastname: Bayeva
authors.forename: Mihai
authors.initials: M
authors.lastname: Gheorghiade
authors.forename: Hossein
authors.initials: H
authors.lastname: Ardehali
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D015195:Drug Design; D004734:Energy Metabolism; D050259:Genes, Mitochondrial; D006321:Heart / Q000503:physiopathology; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D007501:Iron / Q000378:metabolism; D008929:Mitochondria, Heart / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D058990:Molecular Targeted Therapy / Q000379:methods* / Q000639:trends; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000648:ultrastructure; D018384:Oxidative Stress / Q000187:drug effects; D057170:Translational Research, Biomedical / Q000379:methods / Q000639:trends
chemical_list: D002316:Cardiotonic Agents; D007501:Iron