Mitochondria as integrators of signal transduction and energy production in cardiac physiology and disease.
Fascinating links are beginning to be discovered between mitochondrial function and cardiac physiology and disease in the context of diverse signaling mechanisms, energy production, and intersection with pathways producing reactive oxygen species. Proteins long known to drive mitochondrial fusion and fission are now reported to have emergent functions in intracellular calcium homeostasis, apoptosis, and vascular smooth muscle cell proliferation, all key issues in cardiac disease. Moreover, mitochondrial fusion has been demonstrated to be required for normal myofibril organization in skeletal muscle, and decreasing fission may confer protection against ischemic heart disease. These processes broaden the traditional role in energy production undertaken by mitochondria and provide new directions for potential therapeutic leads.
Frohman
Michael A
MA
Department of Pharmacology, Center for Developmental Genetics, Stony Brook University, Stony Brook, NY 11794-5140, USA. michael@pharm.stonybrook.edu
D002318:Cardiovascular Diseases / Q000378:metabolism* / Q000503:physiopathology; D004734:Energy Metabolism; D006321:Heart / Q000502:physiology*; D008561:Membrane Fusion / Q000502:physiology; D008928:Mitochondria / Q000502:physiology* / Q000648:ultrastructure; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology*
D017382:Reactive Oxygen Species