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Aging Effects on Cardiac Progenitor Cell Physiology
Marcello Rota1, Polina Goichberg1, Piero Anversa1
1Departments of Anesthesia and Medicine, and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Insights
Cardiac aging involves changes in cardiac progenitor cells (CPCs), not just aging myocytes. These stem cell alterations contribute to heart failure, but functional CPCs offer potential for stem cell therapy.
Area of Science:
- Cardiovascular Biology
- Gerontology
- Stem Cell Biology
Background:
- The heart was traditionally viewed as a postmitotic organ with a fixed number of myocytes.
- This perspective suggested cardiac cell age matched organismal age, implying homogeneous myocyte populations.
Purpose of the Study:
- To re-evaluate cardiac aging mechanisms in light of cardiac progenitor cell (CPC) discovery.
- To investigate the role of CPC alterations in the development of age-related heart dysfunction (myopathy).
Main Methods:
- Review of existing literature on cardiac aging and stem cell biology.
- Analysis of proposed mechanisms of CPC dysfunction, including self-renewal, differentiation, and telomere shortening.
Main Results:
- Cardiac aging may stem from progressive alterations in CPCs, impacting differentiated cell populations.
- CPC changes include reduced self-renewal, biased differentiation, impaired migration, and senescence.
- Telomere shortening in CPCs is linked to myocardial aging and chronic heart failure.
Conclusions:
- Cardiac progenitor cell dysfunction is a critical factor in human aging myopathy.
- Functionally competent CPCs persist even in failing hearts.
- Stem cell therapy presents a novel therapeutic avenue for age-related heart disease.
Abstract:
Cardiac aging has been confounded by the concept that the heart is a postmitotic organ characterized by a predetermined number of myocytes, which is established at birth and largely preserved throughout life until death of the organ and organism. Based on this premise, the age of cardiac cells should coincide with that of the organism; at any given time, the heart would be composed of a homogeneous population of myocytes of identical age. The discovery that stem cells reside in the heart and generate cardiac cell lineages has imposed a reconsideration of the mechanisms implicated in the manifestations of the aging myopathy. The progressive alterations of terminally differentiated myocytes, and vascular smooth muscle cells and endothelial cells may represent an epiphenomenon dictated by aging effects on cardiac progenitor cells (CPCs). Changes in the properties of CPCs with time may involve loss of self-renewing capacity, increased symmetric division with formation of daughter committed cells, partial depletion of the primitive pool, biased differentiation to the fibroblast fate, impaired ability to migrate, and forced entry into an irreversible quiescent state. Telomere shortening is a major variable of cellular senescence and organ aging, and support the notion that CPCs with critically shortened or dysfunctional telomeres contribute to myocardial aging and chronic heart failure. These defects constitute the critical variables that define the aging myopathy in humans. Importantly, a compartment of functionally competent human CPCs persists in the decompensated heart pointing to stem cell therapy as a novel form of treatment for the aging myopathy.
