Building a new heart from old parts: stem cell turnover in the aging heart

Porrello, Enzo R. and Olson, Eric N. (2010) Building a new heart from old parts: stem cell turnover in the aging heart. Circulation Research, 107 11: 1292-1294. doi:10.1161/CIRCRESAHA.110.235168

Author Porrello, Enzo R.
Olson, Eric N.
Title Building a new heart from old parts: stem cell turnover in the aging heart
Journal name Circulation Research   Check publisher's open access policy
ISSN 0009-7330
Publication date 2010-11-26
Sub-type Editorial
DOI 10.1161/CIRCRESAHA.110.235168
Volume 107
Issue 11
Start page 1292
End page 1294
Total pages 3
Place of publication Baltimore, MD, United States
Publisher Lippincott Williams & Wilkins
Language eng
Formatted abstract
The prevailing dogma in cardiac biology for almost a century has been that the adult mammalian heart is a terminally differentiated organ. According to this paradigm, a 100-year-old human heart is comprised of a population of cardiomyocytes that are as old as the individual. Over the last decade, work from the laboratory of Piero Anversa and others has challenged this dogma.1 Cardiac biologists are now confronted with an alternative conceptual framework proposing the heart as a dynamic, self-renewing organ, capable of cardiomyocyte turnover throughout life.

Heart disease is the leading cause of death in the developed world. A major reason for this is that the adult mammalian heart has limited regenerative capacity following injury. The default healing response to myocyte loss in the adult mammalian heart (eg, following myocardial infarction) involves replacement of myocytes with fibrous, noncontractile scar tissue. The consequent loss of contractile units compromises cardiac function and ultimately leads to heart failure. Absence of regeneration in the adult mammalian heart contrasts with the impressive regenerative potential of lower vertebrates, such as urodele amphibians and teleost fish, which are capable of regenerating significant portions of ventricular myocardium following injury.2,3 Although studies in adult rodents and humans suggest that some myocyte repopulation occurs after myocardial infarction,4,5 this response is clearly limited and incapable of circumventing large-scale myocyte loss, fibrosis, and ultimately organ failure.
Keyword Aging myopathy
Myocyte renewal
Q-Index Code CX
Q-Index Status Provisional Code
Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Editorial
Collection: School of Biomedical Sciences Publications
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