The publication detail shows the title, authors (with indicators showing other profiled authors), information on the publishing organization, abstract and a link to the article in PubMed. This abstract is what is used to create the fingerprint of the publication. If any grants are referenced by the publication, they will be listed here as well.
Mitochondria are sources of metabolic sink and arrhythmias.
Cardiovascular Institute, Mount Sinai School of Medicine, New York, NY 10029, USA. email@example.com
Pharmacology & therapeutics 2011;131(3):287-94.
Mitochondria have long been recognized for their central role in energy transduction and apoptosis. More recently, extensive work in multiple laboratories around the world has significantly extended the role of cardiac mitochondria from relatively static arbitrators of cell death and survival pathways to highly dynamic organelles that form interactive functional networks across cardiomyocytes. These coupled networks were shown to strongly affect cardiomyocyte responses to oxidative stress by modulating cell signaling pathways that strongly impact physiological properties. Of particular importance is the role of mitochondria in modulating key electrophysiological and calcium cycling properties in cardiomyocytes, either directly through activation of a myriad of mitochondrial ion channels or indirectly by affecting cell signaling cascades, ATP levels, and the over-all redox state of the cardiomyocyte. This important recognition has ushered a renewed interest in understanding, at a more fundamental level, the exact role that cardiac metabolism, in general and mitochondria, in particular, play in both health and disease. In this article, we provide an overview of recent advances in our growing understanding of the fundamental role that cardiac mitochondria play in the genesis of lethal arrhythmias.
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