ArticleProceedings of the National Academy of Sciences of the United States of America2006
FGF1/p38 MAP kinase inhibitor therapy induces cardiomyocyte mitosis, reduces scarring, and rescues function after myocardial infarction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
196 citing papers in PubMed, 1 synthesis or guideline pooled it, 366 citations in OpenAlex.
- Cardiac Regeneration: New Insights Into the Frontier of Ischemic Heart Failure Therapy.Frontiers in bioengineering and biotechnology · 2020Pooled it
- Gender-wise distribution of metabolic risk factors and their relationship with fibroblast growth factor 1 and gene polymorphism (rs152524).BMC medical genomics · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.Advanced healthcare materials · 2026Article
- Titin cleavage in living cardiomyocytes induces sarcomere disassembly but does not trigger cell proliferation.The Journal of biological chemistry · 2026Article
- Heart ventricle regeneration in the lizard Eublepharis macularius, the leopard gecko.NPJ Regenerative medicine · 2026Article
- Cell-free strategies for cardiomyocyte proliferation and heart repair.Pharmacological reports : PR · 2026Review
- Harnessing glucocorticoid receptor antagonism to enhance the efficacy of cardiac regenerative growth factors and cytokines.Nature cardiovascular research · 2026Article
- An Exploratory Study of Kinase Activation Profiles in Hypoxic Human Cardiomyocytes Treated with Protective Extracellular Vesicles.Research square · 2026Article
- An infusible decellularized extracellular matrix material binds to vasculature in infarcted myocardium and induces pro-reparative gene expression following acute myocardial infarction through inherent avidity and bioactive signaling.bioRxiv : the preprint server for biology · 2025Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2025Article
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Review
- Rewiring cell identity and metabolism to drive cardiomyocyte proliferation.Cell regeneration (London, England) · 2025Review
- Norepinephrine inhibits cell cycle re-entry of neonatal rat ventricular cardiomyocytes characterized by the absence of de novo nestin expression.Physiological reports · 2025Article
- NestinJournal of cellular physiology · 2025Article
- Revitalizing the heart: strategies and tools for cardiomyocyte regeneration post-myocardial infarction.NPJ Regenerative medicine · 2025Review
- Reversing metabolic reprogramming by CPT1 inhibition with etomoxir promotes cardiomyocyte proliferation and heart regenerationActa pharmaceutica Sinica. B · 2025Article
- Cardiac preservation usingFrontiers in cardiovascular medicine · 2025Article
- Phosphoserine aminotransferase 1 promotes serine synthesis pathway and cardiac repair after myocardial infarction.Theranostics · 2025Article
- Short-term S100A8/A9 Blockade Promotes Cardiac Neovascularization after Myocardial Infarction.Journal of cardiovascular translational research · 2024Article
136 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.