ArticleNature communications2026
Women with polycystic ovary syndrome exhibit impaired endometrial receptivity with excessive ERα and histone lactylation.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed.
- Histone lactylation: a novel epigenetic bridge linking cellular metabolism to benign and malignant gynecological diseases.Clinical epigenetics · 2026Review
- Lactate metabolism and lactylation in female reproductive diseases: From metabolic rewiring to biomarkers and translational therapeutics.Clinical and translational medicine · 2026Review
- Immunological mechanisms of low-grade systemic inflammation and its role in endometrial dysfunction in women with polycystic ovary syndrome.Frontiers in immunology · 2026Article
- Uterine morphology in normogonadotropic anovulation: a comparative study of polycystic ovary syndrome and hypothalamic-pituitary-ovarian dysfunction.Frontiers in endocrinology · 2026Article
- Research progress on protein lactylation in female reproductive disease: molecular mechanisms, functions, and therapeutic implications.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
15 authors.
Funding
Abstract
Polycystic ovary syndrome (PCOS) is one of the most common reproductive disorders in women and severely impairs fertility. Extant clinical studies can only provide indirect and plausible evidence to support endometrial dysfunction as an ovary-independent contributor to PCOS infertility, considering heterogeneous confounders in their phenotypes, comorbidities, and severities. By strictly controlling embryonic factors and potential confounders, our retrospective cohort study reports an adverse implantation rate in women with PCOS, confirming abnormalities in the endometrium, which are accompanied by excessive ERα and histone lactylation. Next, we validate the cooccurrence of impaired uterine receptivity with elevated ERα and histone lactylation in the PCOS mouse model. Inhibiting histone lactylation could downregulate ERα and estrogen-responsive genes, restore uterine receptivity, and improve the implantation rate in PCOS mice. Here, we show that upregulated ERα and histone lactylation are key indicators of impaired endometrial receptivity in PCOS, providing a potential therapeutic strategy by inhibiting lactate production.
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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.