title: Mitochondrial centrality in heart failure.
abstract: A number of observations have shown that mitochondria are at the center of the pathophysiology of the failing heart and mitochondrial-based oxidative stress (OS), myocardial apoptosis, and cardiac bioenergetic dysfunction are implicated in the progression of heart failure (HF), as shown by both clinical studies and animal models. In this manuscript, we review the body of evidence that multiple defects in mitochondria are central and primary to HF progression. In addition, novel approaches to therapeutic targeting of mitochondrial bioenergetic, biogenic, and signaling abnormalities that can impact HF are discussed.
authors.affiliation: The Molecular Cardiology and Neuromuscular Institute, 75 Raritan Ave., Highland Park, NJ 08904, USA. tmci@att.net
authors.forename: José
authors.initials: J
authors.lastname: Marín-García
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Goldenthal
mesh_terms: D000255:Adenosine Triphosphate / Q000096:biosynthesis; D000818:Animals; D017209:Apoptosis; D004734:Energy Metabolism; D006333:Heart Failure / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D008929:Mitochondria, Heart / Q000378:metabolism*; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D000255:Adenosine Triphosphate