The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction
Open accessAbstract
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.
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Cites
Adult Cardiac Stem Cells Are Multipotent and Support Myocardial Regeneration
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Self-citationMolecular Mechanisms of Myocardial Remodeling
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Cited by
Functional screening identifies miRNAs inducing cardiac regeneration
Eulalio, A., Mano, M., Ferro, M. D., Zentilin, L., Sinagra, G., Zacchigna, S., & Giacca, M. (2012) · Nature · doi:10.1038/nature11739 · Cited by 1,029
Hippo–YAP/TAZ signalling in organ regeneration and regenerative medicine
Moya, I. M., & Halder, G. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-018-0086-y · Cited by 981
FGF/FGFR signaling in health and disease
Xie, Y., Su, N., Yang, J., Tan, Q., Huang, S., Jin, M., Ni, Z., Zhang, B., Zhang, D., Luo, F., et al. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00222-7 · Cited by 904
Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair
Kühn, B., del Monte, F., Hajjar, R. J., Chang, Y.-S., Lebeche, D., Arab, S., & Keating, M. T. (2007) · Nature Medicine · doi:10.1038/nm1619 · Cited by 659
Self-citationCardiac Myocyte Cell Cycle Control in Development, Disease, and Regeneration
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Metadata
- Authors
- Engel, F. B., Hsieh, P. C. H., Lee, R. T., & Keating, M. T.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2006-10-17
- Volume
- 103
- Issue
- 42
- Pages
- 15546-15551
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2141376975
- Cited by
- 371
- References
- 29
- FWCI
- 5.40
- Type
- journal article
- Language
- en
- Open access
- green
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- CoChat. (2026). Citation check: FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction. https://app.cochat.ai/papers/10.1073/pnas.0607382103
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- Engel, F. B., Hsieh, P. C. H., Lee, R. T., & Keating, M. T. (2006). FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.0607382103
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