Mitochondrial Targets in Ischaemic Heart Disease and Heart Failure, and their Potential for a More Efficient Clinical Translation. A Scientific Statement of the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardia

Acute myocardial infarction (MI) remains a major cause of death and disability worldwide. No adjuvant treatment has yet been fully validated in patients to limit the progression from the initial tissue damage due to acute MI, to the development of heart failure. However, mitochondria have long been demonstrated to be a key target for cardioprotective strategies to reduce cell death that leads to left ventricular dysfunction and ultimately heart failure. While pre-clinical studies have investigated several mitoprotective strategies targeting different mitochondrial functions, such as oxidative stress or permeability transition pore opening, none have shown successful clinical translation so far. In this European Society of Cardiology scientific statement, we present recent research advances in the understanding of the mitochondrial alterations occurring in MI and in the discovery of key components of mitochondrial structure and function in order to improve drug development. We discuss the reasons for the failure of clinical translation and the remaining obstacles that need to be addressed, including timing of drug administration, tissue bioavailability and efficient mitochondrial targeting, together with the mitochondrial impact derived from risk factors, comorbidities and comedications. Taken together, this scientific statement aims to provides a consensus opinion from clinicians and basic scientists to translate some of the most promising mitoprotective targets into the clinical setting to protect against MI and heart failure.

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Publication Details

Journal
European Journal of Heart Failure
Published
2025-05-04
DOI
https://doi.org/10.1002/ejhf.3674
Citations
9
Primary Topic
Cardiac Ischemia and Reperfusion
Type
article
Field-Weighted Citation Impact
13.24

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article

Mitochondrial Targets in Ischaemic Heart Disease and Heart Failure, and their Potential for a More Efficient Clinical Translation. A Scientific Statement of the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardia

Elizabeth Murphy, Dana Dawson, Ioanna Andreadou, Ange Maguy et al.
9 citations
European Journal of Heart Failure
Cardiac Ischemia and Reperfusion
13.24
article

Mitochondrial Targets in Ischaemic Heart Disease and Heart Failure, and their Potential for a More Efficient Clinical Translation. A Scientific Statement of the ESC Working Group on Cellular Biology of the Heart and the ESC Working Group on Myocardia

Elizabeth Murphy, Dana Dawson, Ioanna Andreadou, Ange Maguy, Jolanda van der Velden, Sean M. Davidson, Derek J. Hausenloy, Cinzia Perrino, Serena Zacchigna, Maurizio Pesce, Rong Tian, Sophie Van Linthout, Peter P. Rainer, Bianca J.J.M. Brundel, Matthias Thielmann, Christoph Maack, Mélanie Paillard, Carlo G. Tocchetti, Petra Kleinbongard, Gemma Chiva‐Blanch, Zoltán Giricz, Luc Bertrand, Katrin Streckfuß‐Bömeke, Christian Bär, Elisa A. Liehn, Paul C. Evans, Mahmoud Abdellatif, Fabio Di Lisa, Frank Lezoualc’h, Thomas Krieg
article en
9 citations

Abstract

Acute myocardial infarction (MI) remains a major cause of death and disability worldwide. No adjuvant treatment has yet been fully validated in patients to limit the progression from the initial tissue damage due to acute MI, to the development of heart failure. However, mitochondria have long been demonstrated to be a key target for cardioprotective strategies to reduce cell death that leads to left ventricular dysfunction and ultimately heart failure. While pre-clinical studies have investigated several mitoprotective strategies targeting different mitochondrial functions, such as oxidative stress or permeability transition pore opening, none have shown successful clinical translation so far. In this European Society of Cardiology scientific statement, we present recent research advances in the understanding of the mitochondrial alterations occurring in MI and in the discovery of key components of mitochondrial structure and function in order to improve drug development. We discuss the reasons for the failure of clinical translation and the remaining obstacles that need to be addressed, including timing of drug administration, tissue bioavailability and efficient mitochondrial targeting, together with the mitochondrial impact derived from risk factors, comorbidities and comedications. Taken together, this scientific statement aims to provides a consensus opinion from clinicians and basic scientists to translate some of the most promising mitoprotective targets into the clinical setting to protect against MI and heart failure.

European Journal of Heart FailureVol. 27(9)
Université Claude Bernard Lyon 1 (FR), Semmelweis University (HU), University of Bern (CH), National Institutes of Health (US), Université Toulouse III - Paul Sabatier (FR), University of Padua (IT), Universitat Oberta de Catalunya (ES), University of Trieste (IT), Inserm (FR), National University of Singapore (SG), Queen Mary University of London (GB), University of Southern Denmark (DK), University of Aberdeen (GB), National and Kapodistrian University of Athens (GR), University of Washington (US), Medical University of Graz (AT), University of Cambridge (GB), Cardiovascular Institute of the South (US), University of Würzburg (DE), King Faisal Specialist Hospital & Research Centre (SA), Instituto de Salud Carlos III (ES), Spanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition (ES), Medizinische Hochschule Hannover (DE), Centro Cardiologico Monzino (IT), Comprehensive Cancer Center Mainfranken (DE), National Heart, Lung, and Blood Institute (US), Amsterdam Neuroscience (NL), Fraunhofer Institute for Toxicology and Experimental Medicine (DE), BioTechMed-Graz (AT), Federico II University Hospital (IT), Universitätsklinikum Würzburg (DE), Duke-NUS Medical School (SG), Laboratoire de recherche en cardiovasculaire, métabolisme, diabétologie et nutrition (FR), Berlin-Brandenburger Centrum für Regenerative Therapien (DE), German Centre for Cardiovascular Research (DE), Berlin Institute of Health at Charité - Universitätsmedizin Berlin (DE), Walloon Excellence in Lifesciences and Biotechnology (BE), National Heart Centre Singapore (SG), Institut des Maladies Métaboliques et Cardiovasculaires (FR), William Harvey Research Institute (GB), Amsterdam University Medical Centers (NL), Consorci Institut D'Investigacions Biomediques August Pi I Sunyer (ES), West German Heart and Vascular Center Essen (DE), University College London (GB), University of Turin (IT), University of Duisburg-Essen (DE), University of Göttingen (DE), MRC Mitochondrial Biology Unit (GB), Vrije Universiteit Amsterdam (NL), International Centre for Genetic Engineering and Biotechnology (IT)
National Science Foundation, Deutsches Zentrum für Herz-Kreislaufforschung, Duke-NUS Medical School, Aromatic Plant Research Center, British Heart Foundation, National Research Foundation, Deutsche Forschungsgemeinschaft, Agence Nationale de la Recherche, Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung, Austrian Science Fund, Fondation pour la Recherche Médicale, Ministero della Salute, Nederlandse Organisatie voor Wetenschappelijk Onderzoek, Schweizerische Herzstiftung, Fondation de France, Karl-Franzens-Universität Graz, Medizinische Universität Graz, EU-CARDIOPROTECTION, BioTechMed-Graz, Fondation Pierre Mercier, Fondation Pierre Mercier pour la Science, HORIZON EUROPE Framework Programme, Medical Research Council, National Medical Research Council
Good health and well-being
Openalex Percentile: Top 1%
Cardiac Ischemia and Reperfusion
13.24
DOIOpen Access PDFOpenAlex
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