ArticleReproductive medicine and biology
Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis.
Article in Reproductive medicine and biology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- The role of fibrosis in endometriosis: a systematic review.Human reproduction update · 2024Pooled it
- Research Progress of Histone Deacetylase and Its Inhibitors in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Epigenetics, Oxidative Stress, and the Microbiome in Endometriosis: Toward an Integrated Mechanistic Framework for Precision Medicine.Journal of personalized medicine · 2026Review
- Gut microbiota composition and systemic immune-inflammatory marker correlations in infertile women with endometriosis: a pilot case-control study.Frontiers in cellular and infection microbiology · 2026Article
- From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.Frontiers in immunology · 2026Review
- Article
- Hypermethylation of Klotho and Peroxisome Proliferator-Activated Receptor γ Concomitant with Overexpression of DNA Methyltransferase 1 in Adenomyosis.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- Gut Microbiota, Circulating Metabolites and Risk of Endometriosis: A Two-Step Mendelian Randomization Study.Polish journal of microbiology · 2024Article
- N-Myc and STAT Interactor is an Endometriosis Suppressor.International journal of molecular sciences · 2024Article
- Aberrant expression of histone deacetylase 8 in endometriosis and its potential as a therapeutic target.Reproductive medicine and biologyArticle
- Corroborating evidence for aberrant expression of histone deacetylase 8 in endometriosis.Reproductive medicine and biologyArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The aim of this study was to evaluate the dynamic change in staining of Class I HDACs and Hdac6 in lesions harvested serially from different time points in mice with induced endometriosis. In addition, the effect of Hdac8 activation as well as Hdac8 and Hdac6 inhibition on lesional progression and fibrogenesis was evaluated. Methods: Immunohistochemistry analysis of Class I HDACs and Hdac6 in serially harvested lesion samples in mouse. Hdac8 activation, as well as Hdac6/8 inhibition, was evaluated in mice with induced endometriosis. Results: We found a progressive increase in lesional staining of Hdac1, Hdac8, and Hdac6 and gradual decrease in Hdac2 staining and consistently reduced staining of Hdac3 during the course of lesional progression. The stromal Hdac8 staining correlated most prominently with all markers of lesional fibrosis. Hdac8 activation significantly accelerated the progression and fibrogenesis of endometriotic lesions. In contrast, specific inhibition of Hdac8 or Hdac6, especially of Hdac8, significantly hindered lesional progression and fibrogenesis. Conclusions: Hdac8 is progressively and aberrantly overexpressed as endometriotic lesions progress. This, along with the documented HDAC1 upregulation in endometriosis and the overwhelming evidence for the therapeutic potentials of HDACIs, calls for further and in-depth investigation of epigenetic aberrations of endometriosis in general and of HDACs in particular.
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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.