Progesterone Actions and Resistance in Gynecological Disorders

Cells · 2022 · vol. 11(4) , pp. 647 · doi:10.3390/cells11040647 · PMID:35203298 · W4213074681
review OA: gold CC0 ⤵ 39 in-corpus citations
AI-generated summary by claude@2026-06, 2026-06-08

This review examines progesterone signaling and resistance in gynecological disorders like endometriosis, adenomyosis, and PCOS, focusing on gene mutations, hormone regulation, and current therapeutic outcomes.

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Abstract

Estrogen and progesterone and their signaling mechanisms are tightly regulated to maintain a normal menstrual cycle and to support a successful pregnancy. The imbalance of estrogen and progesterone disrupts their complex regulatory mechanisms, leading to estrogen dominance and progesterone resistance. Gynecological diseases are heavily associated with dysregulated steroid hormones and can induce chronic pelvic pain, dysmenorrhea, dyspareunia, heavy bleeding, and infertility, which substantially impact the quality of women's lives. Because the menstrual cycle repeatably occurs during reproductive ages with dynamic changes and remodeling of reproductive-related tissues, these alterations can accumulate and induce chronic and recurrent conditions. This review focuses on faulty progesterone signaling mechanisms and cellular responses to progesterone in endometriosis, adenomyosis, leiomyoma (uterine fibroids), polycystic ovary syndrome (PCOS), and endometrial hyperplasia. We also summarize the association with gene mutations and steroid hormone regulation in disease progression as well as current hormonal therapies and the clinical consequences of progesterone resistance.

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Condition tags

endometriosisadenomyosischronic_pelvic_paindysmenorrheadyspareuniainfertility

MeSH descriptors

Leiomyoma Uterine Diseases Endometrium Endometrium Estrogens Female Humans Pregnancy Progesterone

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References (100)

Cited by (39)

Source provenance

europepmc
last seen: 2026-06-04T01:30:01.192114+00:00
openalex
last seen: 2026-06-04T00:00:01.174412+00:00
pubmed
last seen: 2026-05-13T22:23:57.700195+00:00
License: CC0 · commercial use OK