期刊
PHYSIOLOGY
卷 20, 期 -, 页码 303-315出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/physiol.00020.2005
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资金
- NHLBI NIH HHS [P01 HL081427, P01 HL081427-040001, R37 HL054598, P01 HL081427-04, R37 HL054598-10] Funding Source: Medline
Continuous generation of ATP by mitochondrial oxidative phosphorylation is essential to maintain function in mechanically active cells such as cardiomyocytes. Emerging evidence indicates that mitochondrial ion channels activated by reactive oxygen species can induce a mitochondrial critical state, which can scale to cause electrical and contractile dysfunction of the cardiac cell and, ultimately, the whole heart. Here we focus on how mitochondrial ion channels participate in life-and-death decisions of the cell and discuss the challenges ahead for translating recent findings into novel therapeutic applications.
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