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Updated: Mar 30, 2026

Murine Echocardiography of Left Atrium, Aorta, and Pulmonary Artery
Published on: February 20, 2017
[Ageing: a matter of heart?]
Jeanne Mialet-Perez1, Victorine Douin-Echinard1, Daniel Cussac1
1Inserm, UMR1048, institut des maladies métaboliques et cardiovasculaires, 1, avenue Jean Poulhès, BP 84225, 31432 Toulouse cedex 4, France - Université Paul Sabatier, Toulouse, France.
Insights
Ageing accelerates heart failure by promoting cellular senescence in heart cells. This review explores mechanisms like telomere dysfunction and mitochondrial impairment in cardiac ageing.
Area of Science:
- Cardiovascular Biology
- Gerontology
- Cellular Senescence
Background:
- Ageing is a primary risk factor for chronic diseases, with heart failure being significantly impacted.
- Pathological ageing and heart failure are closely intertwined, potentially accelerating each other.
Purpose of the Study:
- To review the mechanisms underlying normal and premature senescence in cardiomyocytes and cardiac stromal cells.
- To elucidate the role of key factors in cardiac ageing and failure.
Main Methods:
- Literature review of recent findings on cellular senescence in the heart.
- Analysis of molecular mechanisms contributing to cardiac ageing.
Main Results:
- Senescence of cardiomyocytes and cardiac stromal cells contributes to heart failure.
- Telomere dysfunction, DNA damage, mitochondrial impairment, miRNAs, and the senescent cell secretome are key players.
Conclusions:
- Cellular senescence is a critical mechanism in cardiac ageing and the development of heart failure.
- Understanding these mechanisms can inform therapeutic strategies for age-related heart disease.
Abstract:
Ageing is considered as a major risk factor for the development of chronic diseases. Among these, heart failure seems to be particularly important for both triggering and accelerating pathological ageing. In the present review, we give a general overview of the most relevant results concerning the mechanism of normal and premature senescence of cardiomyocytes and cardiac stromal cells. In particular, we will address the role of telomere dysfunction, DNA damage response, impairment of mitochondrial function, miRNAs and secretome of senescent cells in cardiac ageing and failure.
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