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

Cardiovasc Res. 2020 Sep 1;116(11):1835-1849. doi: 10.1093/cvr/cvaa132.


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.

Keywords: Animal models; Cardiac ageing; Cardioprotection; Ischaemia/reperfusion injury; Omics.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Age Factors
  • Aging / metabolism
  • Aging / pathology*
  • Animals
  • Cellular Senescence*
  • Disease Models, Animal
  • Extracellular Matrix / metabolism
  • Extracellular Matrix / pathology
  • Heart Disease Risk Factors
  • Heart Diseases / metabolism
  • Heart Diseases / pathology
  • Heart Diseases / physiopathology
  • Heart Diseases / prevention & control*
  • Humans
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology*
  • Phenotype
  • Prognosis
  • Risk Assessment