Cardiomyocyte ageing and cardioprotection: Consensus document from the ESC working groups cell biology of the heart and myocardial function
Ruiz-Meana, Marisol; Bou-Teen, Diana; Ferdinandy, Péter; Gyongyosi, Mariann; Pesce, Maurizio; Perrino, Cinzia; Schulz, Rainer; Sluijter, Joost P.G.; Tocchetti, Carlo G.; Thum, Thomas; Madonna, Rosalinda
(2020) Cardiovascular research, volume 116, issue 11, pp. 1835 - 1849
(Article)
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
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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.
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Keywords: Animal models, Cardiac ageing, Cardioprotection, Ischaemia/reperfusion injury, Omics, Physiology, Cardiology and Cardiovascular Medicine, Physiology (medical)
ISSN: 0008-6363
Publisher: Oxford University Press
Note: Funding Information: This article is based upon work from COST Action EUCARDIOPROTECTION CA16225 supported by COST (European Cooperation in Science and Technology). M.R.M. and D.B.T. are funded by ISCIII (PI19-01196), CIBER-CV, Fundació MTV3-122/C/2015, SEC-2016, and the European Regional Development Fundings (ERDF-FEDER). C.G.T. is supported by a Federico II University/Ricerca di Ateneo grant. R.M. is supported by grants from Incyte s.r.l. and from Ministero dell'Istruzione, Università e Ricerca Scientifica (549901_2020). J.S. is supported by Horizon 2020 ERC-2016-COG EVICARE (725229). P.F. was supported by the National Research, Development and Innovation Office of Hungary (National Heart Program NVKP 16-1-2016-0017) and by the Higher Education Institutional Excellence Program of the Ministry of Human Capacities in Hungary, within the framework of the Therapeutic Devepment thematic program of Semmelweis University. Publisher Copyright: Published on behalf of the European Society of Cardiology. All rights reserved. © The Author(s) 2020.
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