ArticleNature2013
Histone deacetylase 3 coordinates commensal-bacteria-dependent intestinal homeostasis.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 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.
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.
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Who cites it
141 citing papers in PubMed, 240 citations in OpenAlex.
- The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026Review
- Intestinal epithelial memory: from inflammatory imprinting to metabolite-shaped immune tolerance.Barrier immunity · 2026Article
- Intestinal epithelial SETD2 maintains gut microbial homeostasis to attenuate colitis.Clinical and translational medicine · 2026Article
- Tuft cells protect against intestinal inflammation through histone deacetylase 3.Mucosal immunology · 2026Article
- Epigenetic Alterations in Microbiome-Host Interactions in Inflammatory and Autoimmune Diseases.International journal of molecular sciences · 2026Review
- Paneth cell SIRT1 deficiency increases intestinal stress resistance by modulating the gut microbiota.EMBO reports · 2026Article
- Host genetic variation and gut microbiome in pediatric diseases.Chinese medical journal · 2026Review
- Genetics-mediated regulation of intestinal gene expression on microbiome contributes to human disease heritability.Molecular systems biology · 2026Article
- Phytic acid (InsPNature communications · 2026Article
- The interplay of the microbiome, host genetics, and epigenetic modifications in gastric cancer.Frontiers in microbiology · 2026Review
- Gut microbiota and epigenetic inheritance: implications for the development of IBD.Gut microbes · 2025Review
- Butyrate suppresses mucosal inflammation in inflammatory bowel disease primarily through HDAC3 inhibition in monocytes and macrophages.The FEBS journal · 2025Article
- Adiponectin Regulated by Indole-3-Acetic Acid in Paneth Cells Controls Renewal and Differentiation of Gut Stem Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Translational control of innate barrier defense by the gut microbiota.bioRxiv : the preprint server for biology · 2025Article
- NRP1 instructs IL-17-producing ILC3s to drive colitis progression.Cellular & molecular immunology · 2025Article
- Towards Improved Bioavailability of Cereal Inositol Phosphates,Molecules (Basel, Switzerland) · 2025Review
- Chemical interplay between gut microbiota and epigenetics: Implications in circadian biology.Cell chemical biology · 2025Review
- Epigenetic modifications of gut microbiota and their potential role in atherosclerosis.Frontiers in pharmacology · 2025Review
- HDAC3 in action: Expanding roles in inflammation and inflammatory diseases.Cell proliferation · 2025Review
- Review
81 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
21 authors at 1 institution in 1 country.
Funding
Abstract
The development and severity of inflammatory bowel diseases and other chronic inflammatory conditions can be influenced by host genetic and environmental factors, including signals derived from commensal bacteria. However, the mechanisms that integrate these diverse cues remain undefined. Here we demonstrate that mice with an intestinal epithelial cell (IEC)-specific deletion of the epigenome-modifying enzyme histone deacetylase 3 (HDAC3(ΔIEC) mice) exhibited extensive dysregulation of IEC-intrinsic gene expression, including decreased basal expression of genes associated with antimicrobial defence. Critically, conventionally housed HDAC3(ΔIEC) mice demonstrated loss of Paneth cells, impaired IEC function and alterations in the composition of intestinal commensal bacteria. In addition, HDAC3(ΔIEC) mice showed significantly increased susceptibility to intestinal damage and inflammation, indicating that epithelial expression of HDAC3 has a central role in maintaining intestinal homeostasis. Re-derivation of HDAC3(ΔIEC) mice into germ-free conditions revealed that dysregulated IEC gene expression, Paneth cell homeostasis and intestinal barrier function were largely restored in the absence of commensal bacteria. Although the specific mechanisms through which IEC-intrinsic HDAC3 expression regulates these complex phenotypes remain to be determined, these data indicate that HDAC3 is a critical factor that integrates commensal-bacteria-derived signals to calibrate epithelial cell responses required to establish normal host-commensal relationships and maintain intestinal homeostasis.
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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.