ArticleThe Journal of biological chemistry2015
MEF2D deficiency in neonatal cardiomyocytes triggers cell cycle re-entry and programmed cell death in vitro.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- The ADP-ribosyltransferases 3 (ART3) is a novel suppressor of pathological cardiac hypertrophy by ribosylating ITGA7.Acta pharmaceutica Sinica. B · 2026Article
- Lamins gate nuclear and chromatin structures for cardiomyocyte maturation genes.bioRxiv : the preprint server for biology · 2026Article
- The Molecular and Biological Function of MEF2D in Leukemia.Advances in experimental medicine and biology · 2024Review
- Profiling of Chromatin Accessibility in Pigs across Multiple Tissues and Developmental Stages.International journal of molecular sciences · 2023Article
- CRISPR activation and interference as investigative tools in the cardiovascular system.The international journal of biochemistry & cell biology · 2023Article
- Genes of the cGMP-PKG-CaBiochimica et biophysica acta. Molecular basis of disease · 2020Article
- Different class IIa HDACs repressive complexes regulate specific epigenetic responses related to cell survival in leiomyosarcoma cells.Nucleic acids research · 2020Article
- MEF2C repressor variant deregulation leads to cell cycle re-entry and development of heart failure.EBioMedicine · 2020Article
- Effect of Triptolide on Temporal Expression of Cell Cycle Regulators During Cardiac Hypertrophy.Frontiers in pharmacology · 2020Article
- Article
- MEF2 signaling and human diseases.Oncotarget · 2017Review
- Heart Failure and MEF2 Transcriptome Dynamics in Response to β-Blockers.Scientific reports · 2017Article
- Antagonistic regulation of cell-cycle and differentiation gene programs in neonatal cardiomyocytes by homologous MEF2 transcription factors.The Journal of biological chemistry · 2017Article
- Understanding cardiomyocyte proliferation: an insight into cell cycle activity.Cellular and molecular life sciences : CMLS · 2017Review
- MiR-665 regulates VSMCs proliferation via targeting FGF9 and MEF2D and modulating activities of Wnt/β-catenin signaling.American journal of translational research · 2017Article
- The Function of the MEF2 Family of Transcription Factors in Cardiac Development, Cardiogenomics, and Direct Reprogramming.Journal of cardiovascular development and disease · 2016Article
- Signaling Pathways in Cardiac Myocyte Apoptosis.BioMed research international · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The cardiomyocyte cell cycle is a poorly understood process. Mammalian cardiomyocytes permanently withdraw from the cell cycle shortly after birth but can re-enter the cell cycle and proliferate when subjected to injury within a brief temporal window in the neonatal period. Thus, investigating the mechanisms of cell cycle regulation in neonatal cardiomyocytes may provide critical insight into the molecular events that prevent adult myocytes from proliferating in response to injury or stress. MEF2D is a key transcriptional mediator of pathological remodeling in the adult heart downstream of various stress-promoting insults. However, the specific gene programs regulated by MEF2D in cardiomyocytes are unknown. By performing genome-wide transcriptome analysis using MEF2D-depleted neonatal cardiomyocytes, we found a significant impairment in the cell cycle, characterized by the up-regulation of numerous positive cell cycle regulators. Expression of Pten, the primary negative regulator of PI3K/Akt, was significantly reduced in MEF2D-deficient cardiomyocytes and found to be a direct target gene of MEF2D. Consistent with these findings mutant cardiomyocytes showed activation of the PI3K/Akt survival pathway. Paradoxically, prolonged deficiency of MEF2D in neonatal cardiomyocytes did not trigger proliferation but instead resulted in programmed cell death, which is likely mediated by the E2F transcription factor. These results demonstrate a critical role for MEF2D in cell cycle regulation of post-mitotic, neonatal cardiomyocytes in vitro.
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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.