Article thumbnail

Youth is wasted on the young

By Marc S Penn, Martiza E Mayorga and Feng Dong

Abstract

Amphibians and zebrafish are able to regenerate lost myocardial tissue without loss of cardiac function; whereas mammals, in response to myocardial injury, develop scar and lose cardiac function. This dichotomy of response has been thought to be due to the fact that adult mammalian cardiac myocytes are multinucleated and have limited proliferative capacity. Neonatal mammalian cardiac myocytes do have a limited capacity to proliferate. What has been unknown is whether this limited proliferative capacity is associated with the ability to regenerate myocardial tissue soon after birth. Recently, it has been demonstrated that 1-day-old neonatal mice do have the ability to regenerate resected cardiac tissue, and that the capacity to regenerate cardiac tissue is lost by 7 days after birth. The present commentary reviews these results and attempts to offer perspective as to how these important findings relate to current and future strategies to prevent and treat cardiac dysfunction in clinical populations

Topics: Commentary
Publisher: BioMed Central
OAI identifier: oai:pubmedcentral.nih.gov:3152994
Provided by: PubMed Central

To submit an update or takedown request for this paper, please submit an Update/Correction/Removal Request.

Suggested articles

Citations

  1. (2001). Anversa P: Bone marrow cells regenerate infarcted myocardium. Nature
  2. (2001). Anversa P: Evidence that human cardiac myocytes divide after myocardial infarction.
  3. (2001). Anversa P: Mobilized bone marrow cells repair the infarcted heart, improving function and survival.
  4. (2007). Intramyocardial transplantation of autologous CD34+ stem cells for intractable angina: a phase I/IIa double-blind, randomized controlled trial. Circulation
  5. (2002). Keating MT: Heart regeneration in zebrafi sh. Science
  6. (2010). MS: Bone marrow support of the heart in pressure overload is lost with aging. PLoS ONE
  7. (2011). MS: Central role for disabled-2 in mesenchymal stem cardiac protein expression and functional consequences after engraftment in acute myocardial infarction. Stem Cells Dev
  8. (2007). MS: Direct delivery of syngeneic and allogeneic large-scale expanded multipotent adult progenitor cells improves cardiac function after myocardial infarct. Cytotherapy
  9. (2003). MS: Eff ect of stromal-cellderived factor-1 on stem cell homing and tissue regeneration in ischemic cardiomyopathy. Lancet
  10. (2007). MS: SDF-1 expression by mesenchymal stem cells results in trophic support of cardiac myocytes after myocardial infarction.
  11. (2007). MS: SDF-1 recruits cardiac stem cell like cells that depolarize in vivo. Cell Transplant
  12. (2009). RD: Rationale and design for TIME: a phase II, randomized, double-blind, placebo-controlled pilot trial evaluating the safety and eff ect of timing of administration of bone marrow mononuclear cells after acute myocardial infarction. Am Heart J
  13. (2011). Sadek HA: Transient regenerative potential of the neonatal mouse heart. Science
  14. (2010). Simari RD: Intramyocardial injection of autologous bone marrow mononuclear cells for patients with chronic ischemic heart disease and left ventricular dysfunction (First Mononuclear Cells injected in the US [FOCUS]): rationale and design. Am Heart J
  15. (2004). Thymosin β4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair. Nature
  16. (2006). Zeiher AM: Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction.