TY - JOUR
T1 - Targeting mitochondrial fusion and fission proteins for cardioprotection
AU - Hernandez-Resendiz, Sauri
AU - Prunier, Fabrice
AU - Girao, Henrique
AU - Dorn, Gerald
AU - Hausenloy, Derek J.
N1 - Funding Information:
Derek Hausenloy was supported by the British Heart Foundation (CS/14/3/31002), the 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 under its Clinician Scientist‐Senior Investigator scheme (NMRC/CSA‐SI/0011/2017) and Collaborative Centre Grant scheme (NMRC/CGAug16C006), and the Singapore Ministry of Education Academic Research Fund Tier 2 (MOE2016‐T2‐2‐021). Henrique Girao was supported by the European Regional Development Fund (ERDF) through the Operational Program for Competitiveness Factors (COMPETE) [grant numbers PAC ‘NETDIAMOND’ POCI‐01‐0145‐FEDER‐016385, HealthyAging2020 CENTRO‐01‐0145‐FEDER‐000012‐N2323, POCI‐01‐0145‐FEDER‐007440, CENTRO‐01‐0145‐FEDER‐032179, CENTRO‐01‐0145‐FEDER‐032414 and FCTUID/NEU/04539/2013 to CNC.IBILI]. Gerald Dorn was supported by NIH R35 HL135736. This article is based upon work from COST Action EU‐CARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology).
Publisher Copyright:
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd
PY - 2020/6/1
Y1 - 2020/6/1
N2 - New treatments are needed to protect the myocardium against the detrimental effects of acute ischaemia/reperfusion (IR) injury following an acute myocardial infarction (AMI), in order to limit myocardial infarct (MI) size, preserve cardiac function and prevent the onset of heart failure (HF). Given the critical role of mitochondria in energy production for cardiac contractile function, prevention of mitochondrial dysfunction during acute myocardial IRI may provide novel cardioprotective strategies. In this regard, the mitochondrial fusion and fissions proteins, which regulate changes in mitochondrial morphology, are known to impact on mitochondrial quality control by modulating mitochondrial biogenesis, mitophagy and the mitochondrial unfolded protein response. In this article, we review how targeting these inter-related processes may provide novel treatment targets and new therapeutic strategies for reducing MI size, preventing the onset of HF following AMI.
AB - New treatments are needed to protect the myocardium against the detrimental effects of acute ischaemia/reperfusion (IR) injury following an acute myocardial infarction (AMI), in order to limit myocardial infarct (MI) size, preserve cardiac function and prevent the onset of heart failure (HF). Given the critical role of mitochondria in energy production for cardiac contractile function, prevention of mitochondrial dysfunction during acute myocardial IRI may provide novel cardioprotective strategies. In this regard, the mitochondrial fusion and fissions proteins, which regulate changes in mitochondrial morphology, are known to impact on mitochondrial quality control by modulating mitochondrial biogenesis, mitophagy and the mitochondrial unfolded protein response. In this article, we review how targeting these inter-related processes may provide novel treatment targets and new therapeutic strategies for reducing MI size, preventing the onset of HF following AMI.
KW - acute myocardial ischaemia/reperfusion injury
KW - cardioprotection
KW - mitochondrial morphology
KW - mitochondrial unfolded protein response
KW - mitophagy cardioprotection
UR - http://www.scopus.com/inward/record.url?scp=85084457988&partnerID=8YFLogxK
U2 - 10.1111/jcmm.15384
DO - 10.1111/jcmm.15384
M3 - Review article
C2 - 32406208
AN - SCOPUS:85084457988
VL - 24
SP - 6571
EP - 6585
JO - Journal of Cellular and Molecular Medicine
JF - Journal of Cellular and Molecular Medicine
SN - 1582-1838
IS - 12
ER -