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

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 r...

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Bibliografski detalji
Glavni autori: Engel, Felix B., Hsieh, Patrick C. H., Lee, Richard T., Keating, Mark T.
Format: Artigo
Jezik:Inglês
Izdano: National Academy of Sciences 2006
Teme:
Online pristup:https://ncbi.nlm.nih.gov/pmc/articles/PMC1622860/
https://ncbi.nlm.nih.gov/pubmed/17032753
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1073/pnas.0607382103
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