ArticleScientific reports2017
Adult murine cardiomyocytes exhibit regenerative activity with cell cycle reentry through STAT3 in the healing process of myocarditis.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Smarce1-dependent modulation of Stat3 signaling governs cardiomyocyte proliferation.Biological research · 2026Article
- Regenerative therapies for myocardial infarction: exploring the critical role of energy metabolism in achieving cardiac repair.Frontiers in cardiovascular medicine · 2025Review
- Cardiomyocyte Regeneration in Human Myocarditis.Biomedicines · 2024Article
- Chemokine CCL2 promotes cardiac regeneration and repair in myocardial infarction mice via activation of the JNK/STAT3 axis.Acta pharmacologica Sinica · 2024Article
- Yes-associated protein activation potentiates glycogen synthase kinase-3 inhibitor-induced proliferation of neonatal cardiomyocytes and iPS cell-derived cardiomyocytes.Journal of cellular physiology · 2022Article
- IL-6 coaxes cellular dedifferentiation as a pro-regenerative intermediate that contributes to pericardial ADSC-induced cardiac repair.Stem cell research & therapy · 2022Article
- Manipulating Cardiomyocyte Plasticity for Heart Regeneration.Frontiers in cell and developmental biology · 2022Review
- Can polarization of macrophage metabolism enhance cardiac regeneration?Journal of molecular and cellular cardiology · 2021Article
- Induced Cardiomyocyte Proliferation: A Promising Approach to Cure Heart Failure.International journal of molecular sciences · 2021Review
- Mechanisms Underlying Cardiomyocyte Development: Can We Exploit Them to Regenerate the Heart?Current cardiology reports · 2021Review
- Review
- Production of Cardiomyocyte-Like Cells by Fibroblast Reprogramming with Defined Factors.Methods in molecular biology (Clifton, N.J.) · 2021Article
- The pro-apoptosis and pro-inflammation role of LncRNA HIF1A-AS1 in Coxsackievirus B3-induced myocarditis via targeting miR-138.Cardiovascular diagnosis and therapy · 2020Article
- Experimental Rodent Models of Cardiovascular Diseases.Frontiers in cardiovascular medicine · 2020Review
- Review
- Molecular switch model for cardiomyocyte proliferation.Cell regeneration (London, England) · 2019Review
- IL-11 prevents IFN-γ-induced hepatocyte death through selective downregulation of IFN-γ/STAT1 signaling and ROS scavenging.PloS one · 2019Article
- Targeted inhibition of STAT3 as a potential treatment strategy for atherosclerosis.Theranostics · 2019Review
- Senescent cells: a therapeutic target for cardiovascular disease.The Journal of clinical investigation · 2018Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian cardiomyocytes substantially lose proliferative capacity immediately after birth, limiting adult heart regeneration after injury. However, clinical myocarditis appears to be self-limiting with tissue-reparative properties. Here, we investigated the molecular mechanisms underlying the recovery from myocarditis with regard to cardiomyocyte proliferation using an experimental autoimmune myocarditis (EAM) model. Three weeks after EAM induction (EAM3w), cardiac tissue displayed infiltration of inflammatory cells with cardiomyocyte apoptosis. However, by EAM5w, the myocardial damage was remarkably attenuated, associated with an increase in cardiomyocytes that were positively stained with cell cycle markers at EAM3w. Cardiomyocyte fate mapping study revealed that the proliferating cardiomyocytes primarily derived from pre-existing cardiomyocytes. Signal transducer and activator of transcription 3 (STAT3) was robustly activated in cardiomyocytes during inflammation, accompanied by induction of interleukin-6 family cytokines. Cardiomyocyte-specific ablation of STAT3 gene suppressed the frequency of cycling cardiomyocytes in the recovery period without influencing inflammatory status, resulting in impaired tissue repair and cardiac dysfunction. Finally, microarray analysis revealed that the expression of regeneration-related genes, metallothioneins and clusterin, in cardiomyocytes was decreased by STAT3 gene deletion. These data show that adult mammalian cardiomyocytes restore regenerative capacity with cell cycle reentry through STAT3 as the heart recovers from myocarditis-induced cardiac damage.
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