ArticleCirculation research2013
FoxO1 and FoxM1 transcription factors have antagonistic functions in neonatal cardiomyocyte cell-cycle withdrawal and IGF1 gene regulation.
Article in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 102 citations in OpenAlex.
- Dynamic cardiac hyperplasia and hypertrophy in Burmese pythons.American journal of physiology. Cell physiology · 2026Article
- IGF-1 Inhibits the Hemodynamics‑Induced Progression of Intracranial Aneurysms by Modulating the Proliferation and Apoptosis of Vascular Smooth Muscle Cells.Translational stroke research · 2026Article
- MicroRNA networks associated with skeletal aging and WNT pathway modulation.Calcified tissue international · 2026Article
- Cardiac fibroblast Foxm1 deficiency prevents pressure overload-induced cardiac remodeling via the Usp10/MKK6-p38γ MAPK axis.Cell death and differentiation · 2026Review
- Cardiomyocyte-Specific modRNA-Induced FoxM1 Overexpression Promotes Recovery From Myocardial Infarction in Adult Mammals.Circulation · 2026Article
- Oxidized LDL-induced FOXS1 mediates cholesterol transport dysfunction and inflammasome activation to drive aortic valve calcification.Cardiovascular research · 2025Article
- FOXM1 Protects Against Myocardial Ischemia-Reperfusion Injury in Rodent and Porcine Models by Suppressing MKRN1-Dependent LKB1 Ubiquitination.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Myocardial Growth Response to Fetal Intralipid Infusion in Sheep.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- GDF10 promotes rodent cardiomyocyte maturation during the postnatal period.Journal of molecular and cellular cardiology · 2025Article
- The transcriptional repressor Ctbp2 as a metabolite sensor regulating cardiomyocytes proliferation and heart regeneration.Molecular medicine (Cambridge, Mass.) · 2025Article
- FoxO3 controls cardiomyocyte proliferation and heart regeneration by regulating Sfrp2 expression in postnatal mice.Nature communications · 2025Article
- Ontogeny of Fetal Cardiometabolic Pathways: The Potential Role of Cortisol and Thyroid Hormones in Driving the Transition from Preterm to Near-Term Heart Development in Sheep.Journal of cardiovascular development and disease · 2025Article
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- P53 Activation Promotes Maturational Characteristics of Pluripotent Stem Cell-Derived Cardiomyocytes in 3-Dimensional Suspension Culture Via FOXO-FOXM1 Regulation.Journal of the American Heart Association · 2024Article
- Role of transcription factor FOXM1 in diabetes and its complications (Review).International journal of molecular medicine · 2023Article
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part II: Molecular Mechanisms of Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- Alleviating experimental pulmonary hypertensionActa pharmaceutica Sinica. B · 2023Article
- Btg1 and Btg2 regulate neonatal cardiomyocyte cell cycle arrest.Journal of molecular and cellular cardiology · 2023Article
- Foxm1 regulates cardiomyocyte proliferation in adult zebrafish after cardiac injury.Development (Cambridge, England) · 2023Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
rationaleIn the mammalian heart, cardiomyocytes withdraw from the cell cycle and initiate hypertrophic growth soon after birth, but the transcriptional regulatory mechanisms that control these neonatal transitions are not well-defined.
objectiveForkhead family transcription factors have been implicated as positive (forkhead box [Fox] transcription factor M1) and negative (FoxO1 and FoxO3) regulators of cardiomyocyte proliferation prenatally, but their regulatory interactions and functions in neonatal cell-cycle withdrawal have not been reported previously. Potential regulators of Fox activity, including the metabolic indicator AMP-activated protein kinase (AMPK), and Fox transcriptional targets (p21, p27, insulin-like growth factor 1 [IGF1]) also were examined. METHODS AND
resultsIn cultured neonatal rat cardiomyocytes, AMPK activates FoxOs, and AMPK inhibition is sufficient to induce cell proliferation. In vivo, combined loss of FoxO1 and FoxO3 specifically in cardiomyocytes leads to delayed cell-cycle withdrawal and increased expression of IGF1 and FoxM1. Conversely, cardiomyocyte-specific loss of FoxM1 results in decreased neonatal cardiomyocyte cell proliferation, decreased expression of IGF1, and increased expression of cell-cycle inhibitors p21 and p27. IGF1 is a direct downstream target of cardiac Fox transcription factors, which is negatively regulated by FoxOs and positively regulated by FoxM1, dependent on AMPK activation status.
conclusionsThese data support a regulatory mechanism whereby the balance of FoxO and FoxM1 transcription factors integrates metabolic status, mediated by AMPK, and cell-cycle regulation, through competitive regulation of target genes, including IGF1, in neonatal cardiomyocytes.
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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.