ArticleNature communications2023
Cardiomyocyte proliferation is suppressed by ARID1A-mediated YAP inhibition during cardiac maturation.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- A meta-analysis and systematic review of myocardial infarction-induced cardiomyocyte proliferation in adult mouse heart.BMC medicine · 2024Pooled it
- Epigenetic Control of Mammalian Cardiomyocyte Proliferation.Current cardiology reports · 2026Review
- Article
- Cell fate specification during respiratory development requires ARID1A-containing canonical BAF complex activity.Nature communications · 2026Article
- NMRK2-YAP-NADK axis preserves redox protection against myocardial ischemia/reperfusion injury.Redox biology · 2026Article
- MicroRNA-663a upregulation upon ARID1A depletion promotes the growth and migration of esophageal cancer cells by targeting FKBP8.Translational cancer research · 2026Article
- Multi-organ network of cardiometabolic disease-depression multimorbidity revealed by phenotypic and genetic analyses of MR images.Nature communications · 2026Article
- Stress transmission towards the nucleus of the cell.Frontiers in cell and developmental biology · 2026Review
- Engineered Multifunctional Hydrogel Delivering Novel CBX7 Inhibitor Modulates Cuproptosis Via Liquid-Liquid Phase Separation to Restore Cardiac Function in Aged Myocardial Infarction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Molecular gatekeepers of endogenous adult mammalian cardiomyocyte proliferation.Nature reviews. Cardiology · 2025Review
- Review
- The components and regulation of the Hippo pathway and its relationships with the progression and treatment of Non-small cell lung cancer (NSCLC).Cancer cell international · 2025Review
- Tumour initiated purinergic signalling promotes cardiomyocyte RBFOX1 degradation and cardiotoxicity from DNA damaging anticancer agents.Nature communications · 2025Article
- Geometrically controlled cardiac microtissues promote vascularization and reduce inflammationCell biomaterials · 2025Article
- Advanced Microarrays as Heterogeneous Force-Remodeling Coordinator to Orchestrate Nuclear Configuration and Force-Sensing Mechanotransduction in Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Injectable hydrogel with miR-222-engineered extracellular vesicles ameliorates myocardial ischemic reperfusion injury via mechanotransduction.Cell reports. Medicine · 2025Article
- Chronic moderate‑intensity exercise can induce physiological hypertrophy in aged cardiomyocytes through autophagy, with minimal Yap/Taz involvement.Biomedical reports · 2025Article
- Review
- Phosphoserine aminotransferase 1 promotes serine synthesis pathway and cardiac repair after myocardial infarction.Theranostics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inability of adult human cardiomyocytes to proliferate is an obstacle to efficient cardiac regeneration after injury. Understanding the mechanisms that drive postnatal cardiomyocytes to switch to a non-regenerative state is therefore of great significance. Here we show that Arid1a, a subunit of the switching defective/sucrose non-fermenting (SWI/SNF) chromatin remodeling complex, suppresses postnatal cardiomyocyte proliferation while enhancing maturation. Genome-wide transcriptome and epigenome analyses revealed that Arid1a is required for the activation of a cardiomyocyte maturation gene program by promoting DNA access to transcription factors that drive cardiomyocyte maturation. Furthermore, we show that ARID1A directly binds and inhibits the proliferation-promoting transcriptional coactivators YAP and TAZ, indicating ARID1A sequesters YAP/TAZ from their DNA-binding partner TEAD. In ischemic heart disease, Arid1a expression is enhanced in cardiomyocytes of the border zone region. Inactivation of Arid1a after ischemic injury enhanced proliferation of border zone cardiomyocytes. Our study illuminates the pivotal role of Arid1a in cardiomyocyte maturation, and uncovers Arid1a as a crucial suppressor of cardiomyocyte proliferation.
Indexed as
Identifiers
What OpenQuestion holds
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.