Role of stem cells in cardiovascular biology

• Published in: Journal of thrombosis and haemostasis Vol. 9; no. 1; pp. 151 - 161
• Main Authors: HOSODA, T., ROTA, M., KAJSTURA, J., LERI, A., ANVERSA, P.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01-07-2011
• Subjects: aging heart; cardiac niches; cardiac stem cells; Cardiovascular System - cytology; Humans; myocardial regeneration; myocyte turnover; Stem Cells - cytology
• ISSN: 1538-7933; 1538-7836; 1538-7836
• DOI: 10.1111/j.1538-7836.2011.04363.x

This review article addresses the controversy as to whether the adult heart possesses an intrinsic growth reserve. If myocyte renewal takes place in healthy and diseased organs, the reconstitution of the damaged tissue lost upon pathological insults might be achieved by enhancing a natural occurring process. Evidence in support of the old and new view of cardiac biology is critically discussed in an attempt to understand whether the heart is a static or dynamic organ. According to the traditional concept, the heart exerts its function until death of the organism with the same or lesser number of cells that are present at birth. This paradigm was challenged by documentation of the cell cycle activation and nuclear and cellular division in a subset of myocytes. These observations raised the important question of the origin of replicating myocytes. Several theories have been proposed and are presented in this review article. Newly formed myocytes may derive from a pre‐existing pool of cells that has maintained the ability to divide. Alternatively, myocytes may be generated by activation and commitment of resident cardiac stem cells or by migration of progenitor cells from distant organs. In all cases, parenchymal cell turnover throughout lifespan results in a heterogeneous population consisting of young, adult, and senescent myocytes. With time, accumulation of old myocytes has detrimental effects on cardiac performance and may cause the development of an aging myopathy.