Limits...
Regeneration of the heart.

Steinhauser ML, Lee RT - EMBO Mol Med (2011)

Bottom Line: First, although endogenous mammalian cardiac regeneration clearly seems to decline rapidly after birth, it may still persist in adulthood.Second, recent breakthroughs have enabled reprogramming of cells that were apparently terminally differentiated, either by dedifferentiation into pluripotent stem cells or by transdifferentiation into cardiac myocytes.In this review, we discuss the current status of research on cardiac regeneration, with a focus on the challenges that hold back therapeutic development.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Partners Research Building, Cambridge, MA, USA. msteinhauser@partners.org

Show MeSH

Related in: MedlinePlus

The challenge of regenerating the heartBoth exogenously delivered cell therapies and progenitors in the endogenous niche encounter a similar hostile environment after myocardial injury, often including inadequate blood supply (ischemia), inflammation and fibrosis/scarring. Regenerative pathways may be activated by as yet unknown paracrine pathways, responsible for recruiting progenitors from the niche, stimulating proliferation and coaxing differentiation.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3377117&req=5

fig04: The challenge of regenerating the heartBoth exogenously delivered cell therapies and progenitors in the endogenous niche encounter a similar hostile environment after myocardial injury, often including inadequate blood supply (ischemia), inflammation and fibrosis/scarring. Regenerative pathways may be activated by as yet unknown paracrine pathways, responsible for recruiting progenitors from the niche, stimulating proliferation and coaxing differentiation.

Mentions: The plasticity of the mammalian heart and the identification of cell preparations that demonstrate potency for cardiac differentiation has sparked efforts to develop regenerative therapeutic strategies. The therapeutic challenge is considerable: a typical large myocardial infarction that leads to heart failure will kill around 1 billion cardiac myocytes (Laflamme & Murry, 2005), roughly a quarter of the heart's myocytes (Fig 4). A possible therapeutic approach would coax an endogenous stem cell population or an exogenously delivered cell-based therapy to replace lost cardiac myocytes in a coordinated fashion with long-term functional integration. Amongst the myriad of potential cell-based therapies, no clear winning strategy has so far emerged (Segers & Lee, 2008).


Regeneration of the heart.

Steinhauser ML, Lee RT - EMBO Mol Med (2011)

The challenge of regenerating the heartBoth exogenously delivered cell therapies and progenitors in the endogenous niche encounter a similar hostile environment after myocardial injury, often including inadequate blood supply (ischemia), inflammation and fibrosis/scarring. Regenerative pathways may be activated by as yet unknown paracrine pathways, responsible for recruiting progenitors from the niche, stimulating proliferation and coaxing differentiation.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3377117&req=5

fig04: The challenge of regenerating the heartBoth exogenously delivered cell therapies and progenitors in the endogenous niche encounter a similar hostile environment after myocardial injury, often including inadequate blood supply (ischemia), inflammation and fibrosis/scarring. Regenerative pathways may be activated by as yet unknown paracrine pathways, responsible for recruiting progenitors from the niche, stimulating proliferation and coaxing differentiation.
Mentions: The plasticity of the mammalian heart and the identification of cell preparations that demonstrate potency for cardiac differentiation has sparked efforts to develop regenerative therapeutic strategies. The therapeutic challenge is considerable: a typical large myocardial infarction that leads to heart failure will kill around 1 billion cardiac myocytes (Laflamme & Murry, 2005), roughly a quarter of the heart's myocytes (Fig 4). A possible therapeutic approach would coax an endogenous stem cell population or an exogenously delivered cell-based therapy to replace lost cardiac myocytes in a coordinated fashion with long-term functional integration. Amongst the myriad of potential cell-based therapies, no clear winning strategy has so far emerged (Segers & Lee, 2008).

Bottom Line: First, although endogenous mammalian cardiac regeneration clearly seems to decline rapidly after birth, it may still persist in adulthood.Second, recent breakthroughs have enabled reprogramming of cells that were apparently terminally differentiated, either by dedifferentiation into pluripotent stem cells or by transdifferentiation into cardiac myocytes.In this review, we discuss the current status of research on cardiac regeneration, with a focus on the challenges that hold back therapeutic development.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Partners Research Building, Cambridge, MA, USA. msteinhauser@partners.org

Show MeSH
Related in: MedlinePlus