Myocardial aging and senescence: where have the stem cells gone?

Annu Rev Physiol. 2004;66:29-48. doi: 10.1146/annurev.physiol.66.032102.140723.

Abstract

Heart failure remains a leading cause of hospital admissions and mortality in the elderly, and current interventional approaches often fail to treat the underlying cause of pathogenesis. Preservation of structure and function in the aging myocardium is most likely to be successful via ongoing cellular repair and replacement, as well as survival of existing cardiomyocytes that generate contractile force. Research has led to a paradigm shift driven by application of stem cells to generate cardiovascular cell lineages. Early controversial findings of pluripotent precursors adopting cardiac phenotypes are now widely accepted, and current debate centers upon the efficiency of progenitor cell incorporation into the myocardium. Much work remains to be done in determining the relevant progenitor cell population and optimizing conditions for efficient differentiation and integration. Significant implications exist for treatment of pathologically damaged or aging myocardium since future interventional approaches will capitalize upon the use of cardiac stem cells as therapeutic reagents.

Publication types

  • Review

MeSH terms

  • Aging / physiology*
  • Animals
  • Cell Division
  • Heart / growth & development*
  • Humans
  • Myocardium / cytology*
  • Myocardium / enzymology
  • Myocardium / metabolism
  • Protein-Serine-Threonine Kinases*
  • Proto-Oncogene Proteins / physiology
  • Proto-Oncogene Proteins c-akt
  • Stem Cells / cytology*
  • Telomerase / metabolism
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Proto-Oncogene Proteins
  • Tumor Suppressor Protein p53
  • Protein-Serine-Threonine Kinases
  • Proto-Oncogene Proteins c-akt
  • Telomerase