Mitochondria, the calcium uniporter, and reperfusion-induced ventricular fibrillation.
The role of the mitochondria, and in particular the calcium (Ca) uniporter, in mediating reperfusion-induced arrhythmias is a novel investigative area. This commentary assesses the importance of a new article on this topic, published in this issue of the journal. Ventricular arrhythmogenesis remains an important area of research in the search of novel targets. The article by García-Rivas et al in this issue represents a possible novel focus for investigation.
Clements-Jewery
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Department of Physiology, Loyola University Medical Center, Maywood, IL 60153, USA. hclementsjewery@lumc.edu
D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D033681:Mitochondrial Membrane Transport Proteins / Q000378:metabolism; D000083162:Mitochondrial Permeability Transition Pore; D015425:Myocardial Reperfusion / Q000009:adverse effects*; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism; D017975:Ruthenium Compounds / Q000494:pharmacology; D014693:Ventricular Fibrillation / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; C112020:Ru 360; D017975:Ruthenium Compounds; C034703:mitochondrial calcium uniporter