期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 78, 期 -, 页码 46-53出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2014.10.013
关键词
Mitochondria; Calcium; Necrosis; Ischemia-reperfusion; Mitochondrial permeability pore
资金
- NHLBI [ZIA HL002066]
- National Institutes of Health (NIH) Medical Research Scholars Program [ZIA HL002065]
- NIH
Calcium is of critical importance to mitochondrial and cell function, and calcium signaling is highly localized in the cell. When stimulated, mitochondria are capable of rapidly taking up calcium, affecting both matrix energetics within mitochondria and shaping the amplitude and frequency of cytosolic calcium waves. During pathological conditions a large increase in mitochondrial calcium levels is thought to activate the mitochondrial permeability transition pore, resulting in cell death. The protein responsible for mitochondrial calcium uptake, the mitochondrial calcium uniporter (MCU), was identified in 2011 and its molecular elucidation has stimulated and invigorated research in this area. MCU knockout mice have been created, a variety of other regulators have been identified, and a disease phenotype in humans has been attributed to the loss of a uniporter regulator. In the three years since its molecular elucidation, further research into the MCU has revealed a complex uniporter, and raised many questions about its physiologic and pathologic cell roles. This article is part of a Special Issue entitled Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease. Published by Elsevier Ltd.
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