ArticleDevelopment (Cambridge, England)2017
Sin3a regulates epithelial progenitor cell fate during lung development.
Article in Development (Cambridge, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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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.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
- BRD4 promotes endodermal cell fate during mammalian lung development.JCI insight · 2026Article
- Sotatercept Reverses SIN3a Deficiency-Driven PAH by Reprogramming BMPR2/TGF-β-HIF-1α Signaling Pathways.bioRxiv : the preprint server for biology · 2026Article
- Comparative transcriptomics reveal the common anteroposterior molecular blueprint of adult bilaterian guts.PLoS biology · 2026Article
- Hierarchical regulation of cerebellar neurogenesis by Sin3A-mediated gene repression.bioRxiv : the preprint server for biology · 2025Article
- Progressive lung fibrosis: reprogramming a genetically vulnerable bronchoalveolar epithelium.The Journal of clinical investigation · 2025Review
- Rescuing lung development through embryonic inhibition of histone acetylation.Science translational medicine · 2024Article
- T-regulatory cells require Sin3a for stable expression of Foxp3.Frontiers in immunology · 2024Article
- Switch-Independent 3A: An Epigenetic Regulator in Cancer with New Implications for Pulmonary Arterial Hypertension.Biomedicines · 2023Review
- Age-associated H3K9me2 loss alters the regenerative equilibrium between murine lung alveolar and bronchiolar progenitors.Developmental cell · 2023Article
- SIN-3 acts in distinct complexes to regulate the germline transcriptional program in Caenorhabditis elegans.Development (Cambridge, England) · 2023Article
- Epithelial Yap/Taz are required for functional alveolar regeneration following acute lung injury.JCI insight · 2023Article
- SAP30 promotes breast tumor progression by bridging the transcriptional corepressor SIN3 complex and MLL1.The Journal of clinical investigation · 2023Article
- An Overfeeding-Induced Obesity Mouse Model Reveals Necessity for Sin3a in Postnatal Peak β-Cell Mass Acquisition.Diabetes · 2022Article
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- Sin3a drives mesenchymal-to-epithelial transition through cooperating with Tet1 in somatic cell reprogramming.Stem cell research & therapy · 2022Article
- Cellular Senescence: Pathogenic Mechanisms in Lung Fibrosis.International journal of molecular sciences · 2021Review
- Senescence of Alveolar Type 2 Cells Drives Progressive Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021Article
- SIN3A Regulates Porcine Early Embryonic Development by ModulatingFrontiers in cell and developmental biology · 2021Article
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- Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Mechanisms that regulate tissue-specific progenitors for maintenance and differentiation during development are poorly understood. Here, we demonstrate that the co-repressor protein Sin3a is crucial for lung endoderm development. Loss of Sin3a in mouse early foregut endoderm led to a specific and profound defect in lung development with lung buds failing to undergo branching morphogenesis and progressive atrophy of the proximal lung endoderm with complete epithelial loss at later stages of development. Consequently, neonatal pups died at birth due to respiratory insufficiency. Further analysis revealed that loss of Sin3a resulted in embryonic lung epithelial progenitor cells adopting a senescence-like state with permanent cell cycle arrest in G1 phase. This was mediated at least partially through upregulation of the cell cycle inhibitors Cdkn1a and Cdkn2c. At the same time, loss of endodermal Sin3a also disrupted cell differentiation of the mesoderm, suggesting aberrant epithelial-mesenchymal signaling. Together, these findings reveal that Sin3a is an essential regulator for early lung endoderm specification and differentiation.
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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.