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Proc Natl Acad Sci U S A. 2006 Oct 17;103(42):15546-51. Epub 2006 Oct 10.

FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction.

Author information

1
Department of Pediatrics, Harvard Medical School, Children's Hospital, 320 Longwood Avenue, Boston, MA 02115, USA. engel@enders.tch.harvard.edu

Abstract

Mammalian cardiomyocytes have limited proliferation potential, and acutely injured mammalian hearts do not regenerate adequately. Instead, injured myocardium develops fibrosis and scarring. Here we show that FGF1/p38 MAP kinase inhibitor treatment after acute myocardial injury in 8- to 10-week-old rats increases cardiomyocyte mitosis. At 3 months after injury, 4 weeks of FGF1/p38 MAP kinase inhibitor therapy results in reduced scarring and wall thinning, with markedly improved cardiac function. In contrast, p38 MAP kinase inhibition alone fails to rescue heart function despite increased cardiomyocyte mitosis. FGF1 improves angiogenesis, possibly contributing to the survival of newly generated cardiomyocytes. Our data indicate that FGF1 and p38 MAP kinase, proteins involved in cardiomyocyte proliferation and angiogenesis during development, may be delivered therapeutically to enhance cardiac regeneration.

PMID:
17032753
PMCID:
PMC1622860
DOI:
10.1073/pnas.0607382103
[Indexed for MEDLINE]
Free PMC Article
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