Cardiomyocyte ageing and cardioprotection: consensus document from the ESC working groups cell biology of the heart and myocardial function

Author:

Ruiz-Meana Marisol1,Bou-Teen Diana1,Ferdinandy Péter23,Gyongyosi Mariann4ORCID,Pesce Maurizio5ORCID,Perrino Cinzia6ORCID,Schulz Rainer7,Sluijter Joost P G89ORCID,Tocchetti Carlo G10,Thum Thomas11ORCID,Madonna Rosalinda1213

Affiliation:

1. Department of Cardiology, Hospital Universitari Vall d’Hebron, Vall d’Hebron Institut de Recerca (VHIR), Universitat Autonoma de Barcelona and Centro de Investigación Biomédica en Red-CV, CIBER-CV, Madrid, Spain

2. Department of Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary

3. Pharmahungary Group, Szeged, Hungary

4. Department of Cardiology, Medical University of Vienna, Waehringer Guertel 18-20, A-1090 Vienna, Austria

5. Unità di Ingegneria Tissutale Cardiovascolare, Centro Cardiologico Monzino, IRCCS, Milan, Italy

6. Department of Advanced Biomedical Sciences, Federico II University, Naples, Italy

7. Institute of Physiology, Justus-Liebig University Giessen, Giessen, Germany

8. Laboratory of Experimental Cardiology, Department of Cardiology, University Medical Center Utrecht, Utrecht, The Netherlands

9. Circulatory Health Laboratory, Regenerative Medicine Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands

10. Department of Translational Medical Sciences and Interdepartmental Center of Clinical and Translational Sciences (CIRCET), Federico II University, Naples, Italy

11. Institute for Molecular and Translational Therapeutic Strategies (IMTTS), Hannover Medical School, Hannover, Germany

12. Institute of Cardiology, University of Pisa, Pisa, Italy

13. Department of Internal Medicine, University of Texas Medical School in Houston, Houston, TX, USA

Abstract

Abstract Advanced age is a major predisposing risk factor for the incidence of coronary syndromes and comorbid conditions which impact the heart response to cardioprotective interventions. Advanced age also significantly increases the risk of developing post-ischaemic adverse remodelling and heart failure after ischaemia/reperfusion (IR) injury. Some of the signalling pathways become defective or attenuated during ageing, whereas others with well-known detrimental consequences, such as glycoxidation or proinflammatory pathways, are exacerbated. The causative mechanisms responsible for all these changes are yet to be elucidated and are a matter of active research. Here, we review the current knowledge about the pathophysiology of cardiac ageing that eventually impacts on the increased susceptibility of cells to IR injury and can affect the efficiency of cardioprotective strategies.

Funder

COST Action EU-CARDIOPROTECTION

COST

European Cooperation in Science and Technology

ISCIII

European Regional Development Fundings

Federico II University

Ricerca di Ateneo

Incyte s.r.l. and from Ministero dell’Istruzione

Università e Ricerca Scientifica

National Research, Development and Innovation Office of Hungary

National Heart Program

Higher Education Institutional Excellence Program

Ministry of Human Capacities in Hungary

Therapeutic Devepment

Semmelweis University

Publisher

Oxford University Press (OUP)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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