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Mitochondrial ion channels as targets for cardioprotection

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

  1. COST (European Cooperation in Science and Technology) [CA16225]
  2. British Heart Foundation [CS/14/3/31002]
  3. National Institute for Health Research University College London Hospitals Biomedical Research Centre
  4. Duke-National University Singapore Medical School
  5. Singapore Ministry of Health's National Medical Research Council [NMRC/CSA-SI/0011/2017, NMRC/CGAug16C006]
  6. Singapore Ministry of Education Academic Research Fund Tier 2 [MOE2016-T2-2-021]
  7. Leducq Transatlantic Network of Excellence [16CVD04]
  8. Swiss National Science Foundation [310030E_176050, IZCOZ0_189878]
  9. MRC [MR/J003530/1] Funding Source: UKRI
  10. Swiss National Science Foundation (SNF) [310030E_176050, IZCOZ0_189878] Funding Source: Swiss National Science Foundation (SNF)

向作者/读者索取更多资源

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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