Role of HOXA10 in pathologies of the endometrium

Anuradha Mishra, Deepak Modi
Reviews in endocrine & metabolic disorders · 2024 · vol. 26(1) , pp. 81–96 · doi:10.1007/s11154-024-09923-8 · PMID:39499452 · W4404085063
review OA: closed CC0 ⤵ 2 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06+body, 2026-06-07 ⓘ

HOXA10 is crucial for uterine functions, and its dysregulation, caused by genetic changes or pollutants, leads to endometrial pathologies and infertility by affecting cell proliferation and signaling.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper reviews evidence that the transcription factor HOXA10 is critical for uterine development, endometrial receptivity, implantation, and stromal decidualization, and that its expression becomes dysregulated in multiple endometrial disorders including adenomyosis and endometriosis. It synthesizes findings from genetic, epigenetic (DNA methylation), microRNA-mediated, and environmental pollutant/endocrine disruptor mechanisms, alongside in vivo mouse and in vitro human cell studies, reporting that HOXA10 downregulation leads to increased epithelial proliferation, impaired stromal decidualization, and altered cell-cycle, immune, and signaling pathways. A key limitation is that much of the evidence is mechanistic and drawn from heterogeneous models and disorder contexts rather than a single prospective dataset. This paper is centrally about endometriosis and adenomyosis — it summarizes HOXA10 dysregulation as a shared mechanistic theme across these endometrial pathologies.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

HOXA10 belongs to the homeobox gene family and is essential for uterine biogenesis, endometrial receptivity, embryo implantation, and stromal cell decidualization. Available evidence suggests that the expression of HOXA10 is dysregulated in different endometrial disorders like endometrial hyperplasia, endometrial cancer, adenomyosis, endometriosis, recurrent implantation failure, and unexplained infertility. The downregulation of HOXA10 occurs by genetic changes in the HOXA10 gene, methylation of the HOXA10 locus, or selected miRNAs. Endocrine disruptors and organic pollutants also cause the reduced expression of HOXA10 in these conditions. In vivo experiments in mouse models and in vitro studies in human cell lines demonstrate that downregulation of HOXA10 leads to endometrial epithelial cell proliferation, failure of stromal cell decidualization, altered expression of genes involved in cell cycle regulation, immunomodulation, and various signaling pathways. These disruptions are speculated to cause infertility associated with the disorders of the endometrium.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Endometrium Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins Homeodomain Proteins

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (100)

Cited by (2)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-06-11T06:17:07.201654+00:00
License: CC0 · commercial use OK