ArticleNature communications2022
Lamin A/C-dependent chromatin architecture safeguards naïve pluripotency to prevent aberrant cardiovascular cell fate and function.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- The cardiac 4D nucleome: nuclear and chromatin dynamics across development, disease and ageing.Nature reviews. Cardiology · 2026Review
- InstaNovo-P: a de novo peptide sequencing model for phosphoproteomics.Nature communications · 2026Article
- Single Cell Mechanics in Disease Progression.Small science · 2026Review
- Lamins gate nuclear and chromatin structures for cardiomyocyte maturation genes.bioRxiv : the preprint server for biology · 2026Article
- Gene-gene interactions between a LMNA variant and common polymorphisms drive early-onset atrial fibrillation.Nature communications · 2026Article
- Review
- Nuclear Lamins: A Molecular Bridge Coupling Extracellular Mechanical Cues to Intranuclear Signal Transduction and Gene Regulation.International journal of molecular sciences · 2026Review
- Epigenetics, Modifiers, and Molecular Noise: Rethinking Pathophysiology in Dilated and Hypertrophic Cardiomyopathies.International journal of molecular sciences · 2026Review
- Hat1 Orchestrates Heterochromatin Inheritance by Regulating Localization of H3K9 Methyltransferases.bioRxiv : the preprint server for biology · 2026Article
- Lamin A/C as a Molecular Link Between Nuclear Organization, Chromatin Dynamics, and Tumor Progression.Cells · 2026Review
- Lamin A/C-regulated cysteine catabolic flux modulates stem cell fate through epigenome reprogramming.Nature metabolism · 2026Article
- Methylation, acetylation and cell fate.Nature metabolism · 2026Article
- The Regulatory Role of mCells · 2026Review
- Lamin A/C maintains genome topology and regulates transcriptional programs essential for virus-driven B cell activation.bioRxiv : the preprint server for biology · 2026Article
- Phosphorylation-dependent modulation of the Lamin A/C-EZH2 complex regulates epithelial-mesenchymal plasticity.Nucleic acids research · 2026Article
- Lamin A/C directs nucleosome-scale chromatin remodeling to define early lineage segregation in mammals.bioRxiv : the preprint server for biology · 2026Article
- A Mechano-Feedback Loop Orchestrated by SUN1/2 Governs Cellular Mechanoadaptation via Lamina-Associated Domain Remodeling.Research (Washington, D.C.) · 2026Article
- Mechanosensitive snoRNA-like circular RNA sno-circCNOT1 drives endothelial dysfunction and atherosclerosis.Theranostics · 2026Article
- Nuclear destabilisation - a possible genesis of cancer?Biological reviews of the Cambridge Philosophical Society · 2025Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
Corrections and comments
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tight control of cell fate choices is crucial for normal development. Here we show that lamin A/C plays a key role in chromatin organization in embryonic stem cells (ESCs), which safeguards naïve pluripotency and ensures proper cell fate choices during cardiogenesis. We report changes in chromatin compaction and localization of cardiac genes in Lmna-/- ESCs resulting in precocious activation of a transcriptional program promoting cardiomyocyte versus endothelial cell fate. This is accompanied by premature cardiomyocyte differentiation, cell cycle withdrawal and abnormal contractility. Gata4 is activated by lamin A/C loss and Gata4 silencing or haploinsufficiency rescues the aberrant cardiovascular cell fate choices induced by lamin A/C deficiency. We uncover divergent functions of lamin A/C in naïve pluripotent stem cells and cardiomyocytes, which have distinct contributions to the transcriptional alterations of patients with LMNA-associated cardiomyopathy. We conclude that disruption of lamin A/C-dependent chromatin architecture in ESCs is a primary event in LMNA loss-of-function cardiomyopathy.
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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 Socratic graph.