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.
| Original language | English |
|---|---|
| Pages (from-to) | 1835-1849 |
| Number of pages | 15 |
| Journal | Cardiovascular research |
| Volume | 116 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - 1 Sept 2020 |
Keywords
- Animal models
- Cardiac ageing
- Cardioprotection
- Ischaemia/reperfusion injury
- Omics
Fingerprint
Dive into the research topics of 'Cardiomyocyte ageing and cardioprotection: Consensus document from the ESC working groups cell biology of the heart and myocardial function'. Together they form a unique fingerprint.Cite this
- APA
- Author
- BIBTEX
- Harvard
- Standard
- RIS
- Vancouver