Senescence mechanisms and targets in the heart
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Updated: Nov 6, 2025
Viral Transgene Expression in Rodent Hearts and the Assessment of Cardiac Arrhythmia Risk
Published on: July 27, 2022
Maggie S Chen1, Richard T Lee1,2, Jessica C Garbern1,3
1Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, 7 Divinity Ave, Cambridge, MA 02138, USA.
Abstract:
Cellular senescence is a state of irreversible cell cycle arrest associated with ageing. Senescence of different cardiac cell types can direct the pathophysiology of cardiovascular diseases (CVDs) such as atherosclerosis, myocardial infarction, and cardiac fibrosis. While age-related telomere shortening represents a major cause of replicative senescence, the senescent state can also be induced by oxidative stress, metabolic dysfunction, and epigenetic regulation, among other stressors. It is critical that we understand the molecular pathways that lead to cellular senescence and the consequences of cellular senescence in order to develop new therapeutic approaches to treat CVD. In this review, we discuss molecular mechanisms of cellular senescence, explore how cellular senescence of different cardiac cell types (including cardiomyocytes, cardiac endothelial cells, cardiac fibroblasts, vascular smooth muscle cells, and valve interstitial cells) can lead to CVD, and highlight potential therapeutic approaches that target molecular mechanisms of cellular senescence to prevent or treat CVD.
Insights
Cellular senescence, a key aging process, drives cardiovascular diseases (CVDs). Understanding senescence mechanisms offers new therapeutic targets for preventing and treating conditions like atherosclerosis and heart attack.
Area of Science:
- Cardiovascular Biology
- Cellular Aging
- Molecular Medicine
Background:
- Cellular senescence is irreversible cell cycle arrest linked to aging.
- Senescence in cardiac cells contributes to cardiovascular diseases (CVDs) like atherosclerosis and myocardial infarction.
- Triggers include telomere shortening, oxidative stress, and metabolic dysfunction.
Purpose of the Study:
- To review molecular mechanisms of cellular senescence.
- To explore the role of senescent cardiac cells in CVD.
- To highlight therapeutic strategies targeting senescence for CVD treatment.
Main Methods:
- Literature review of cellular senescence.
- Analysis of senescence in various cardiac cell types (cardiomyocytes, endothelial cells, fibroblasts, etc.).
- Discussion of therapeutic targets for senescence-related CVD.
Main Results:
- Cellular senescence is a significant contributor to CVD pathophysiology.
- Specific cardiac cell types undergo senescence, exacerbating disease progression.
- Targeting senescence pathways presents promising therapeutic avenues.
Conclusions:
- Understanding senescence mechanisms is crucial for developing novel CVD therapies.
- Targeting cellular senescence holds potential for preventing and treating age-related cardiovascular conditions.
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