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Updated: Jun 28, 2025
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Published on: February 20, 2017
The Senescent Heart-"Age Doth Wither Its Infinite Variety"
Anupama Vijayakumar1, Mingyi Wang2, Shivakumar Kailasam3
1Cardiovascular Genetics Laboratory, Department of Biotechnology, Bhupat and Jyothi Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036, India.
Insights
Aging significantly increases cardiovascular disease risk by altering cardiac fibroblast function. Discoidin domain receptor 2 (DDR2) is a key factor in senescent heart fibrosis, offering potential therapeutic targets.
Area of Science:
- Cardiovascular biology
- Aging research
- Fibrosis mechanisms
Background:
- Cardiovascular diseases (CVDs) are a major global health burden, with aging as a primary risk factor.
- Cardiac aging involves cellular changes and reduced regeneration, impacting myocardial integrity.
- Dysregulated signaling in cardiac fibroblasts is increasingly linked to cardiovascular aging and fibrosis.
Purpose of the Study:
- To investigate the role of cardiac fibroblast-specific factors in the aging heart.
- To explore the mechanisms underlying cardiac fibroblast dysfunction in senescence.
- To identify potential therapeutic targets for mitigating age-related cardiovascular disease.
Main Methods:
- Analysis of molecular mechanisms in cardiac fibroblasts during aging.
- Investigating the function of Discoidin domain receptor 2 (DDR2) in senescent myocardium.
- Characterizing the role of DDR2 in cardiovascular fibrosis.
Main Results:
- Recent studies highlight the critical role of cardiac fibroblasts in cardiovascular aging.
- Discoidin domain receptor 2 (DDR2), a collagen-activated receptor tyrosine kinase, is predominantly expressed in cardiac fibroblasts.
- DDR2 plays an essential role in cardiac fibroblast function and the development of cardiovascular fibrosis.
Conclusions:
- Understanding molecular mechanisms in senescent cardiac fibroblasts is crucial for addressing age-related CVDs.
- DDR2 is a key regulator of cardiac fibroblast function and fibrosis in the aging heart.
- Targeting DDR2 may offer novel strategies to combat cardiovascular diseases in the elderly population.
Abstract:
Cardiovascular diseases are a leading cause of morbidity and mortality world-wide. While many factors like smoking, hypertension, diabetes, dyslipidaemia, a sedentary lifestyle, and genetic factors can predispose to cardiovascular diseases, the natural process of aging is by itself a major determinant of the risk. Cardiac aging is marked by a conglomerate of cellular and molecular changes, exacerbated by age-driven decline in cardiac regeneration capacity. Although the phenotypes of cardiac aging are well characterised, the underlying molecular mechanisms are far less explored. Recent advances unequivocally link cardiovascular aging to the dysregulation of critical signalling pathways in cardiac fibroblasts, which compromises the critical role of these cells in maintaining the structural and functional integrity of the myocardium. Clearly, the identification of cardiac fibroblast-specific factors and mechanisms that regulate cardiac fibroblast function in the senescent myocardium is of immense importance. In this regard, recent studies show that Discoidin domain receptor 2 (DDR2), a collagen-activated receptor tyrosine kinase predominantly located in cardiac fibroblasts, has an obligate role in cardiac fibroblast function and cardiovascular fibrosis. Incisive studies on the molecular basis of cardiovascular aging and dysregulated fibroblast function in the senescent heart would pave the way for effective strategies to mitigate cardiovascular diseases in a rapidly growing elderly population.
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