期刊
JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
卷 24, 期 13, 页码 7102-7114出版社
WILEY
DOI: 10.1111/jcmm.15341
关键词
acute ischaemia; reperfusion injury; cardioprotection; Mitochondria; mitochondrial permeability transition pore
资金
- COST (European Cooperation in Science and Technology) [CA16225]
- British Heart Foundation [CS/14/3/31002]
- National Institute for Health Research University College London Hospitals Biomedical Research Centre
- Duke-National University Singapore Medical School
- Singapore Ministry of Health's National Medical Research Council [NMRC/CSA-SI/0011/2017, NMRC/CGAug16C006]
- Singapore Ministry of Education Academic Research Fund Tier 2 [MOE2016-T2-2-021]
- Leducq Transatlantic Network of Excellence [16CVD04]
- Swiss National Science Foundation [310030E_176050, IZCOZ0_189878]
- MRC [MR/J003530/1] Funding Source: UKRI
- Swiss National Science Foundation (SNF) [310030E_176050, IZCOZ0_189878] Funding Source: Swiss National Science Foundation (SNF)
Acute myocardial infarction (AMI) and the heart failure (HF) that often result remain the leading causes of death and disability worldwide. As such, new therapeutic targets need to be discovered to protect the myocardium against acute ischaemia/reperfusion (I/R) injury in order to reduce myocardial infarct (MI) size, preserve left ventricular function and prevent the onset of HF. Mitochondrial dysfunction during acute I/R injury is a critical determinant of cell death following AMI, and therefore, ion channels in the inner mitochondrial membrane, which are known to influence cell death and survival, provide potential therapeutic targets for cardioprotection. In this article, we review the role of mitochondrial ion channels, which are known to modulate susceptibility to acute myocardial I/R injury, and we explore their potential roles as therapeutic targets for reducing MI size and preventing HF following AMI.
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