Role of Steroid Hormones: Progesterone Signaling

In: Endometriosis · 2011 · pp. 145–152 · doi:10.1002/9781444398519.ch14 · W1599802071
other OA: closed CC0 ⤵ 2 in-corpus citations
View on OpenAlex View at publisher
AI-generated summary by claude@2026-06, 2026-06-09

This paper investigates how progesterone receptor activity regulates reproductive tissue remodeling and how disruptions in this signaling, known as progesterone resistance, are linked to endometriosis and epigenetic changes.

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

Abstract

Key reproductive events, including ovulation, implantation and menstruation, are dependent upon cyclic tissue remodeling, characterized by waves of cell proliferation, differentiation, recruitment of inflammatory cells, apoptosis, tissue breakdown, and regeneration. The progesterone receptor, a member of the superfamily of ligand-dependent transcription factors, is the master regulator of cycle-dependent tissue remodeling in the reproductive tract and its activity is tightly regulated by interaction with cell-specific co-regulators and post-translational modifications that respond dynamically to a variety of environmental and inflammatory signals. Endometriosis, a chronic inflammatory disorder, disrupts co-ordinated progesterone responses throughout the reproductive tract, although most prominently in the endometrium. This phenomenon is increasingly referred to as "progesterone resistance." Emerging evidence suggests that progesterone resistance in endometriosis is not just a consequence of perturbed progesterone signal transduction caused by chronic inflammation but associated with long-lasting epigenetic reprogramming of the steroid hormone responses in the endometrium and beyond.

My notes (saved in your browser only)

Condition tags

endometriosis

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 (65)

Cited by (2)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC0 · commercial use OK