Progesterone resistance in endometriosis: origins, consequences and interventions
Abstract
Endometriosis is a common cause of pelvic pain and affects up to 10% of women of reproductive age. Aberrant progesterone signaling in the endometrium plays a significant role in impaired decidualization and establishment of ectopic endometrial implants. Eutopic endometrial cells from women with endometriosis fail to downregulate genes needed for decidualization, such as those involved in cell cycle regulation, leading to unbridled proliferation. Several causes of progesterone resistance in the endometrium have been postulated, including congenital "preconditioning", whereby the in utero environment renders infants susceptible to neonatal uterine bleeding and endometriosis. Progesterone action is crucial to decreasing inflammation in the endometrium, and deviant progesterone signaling results in a proinflammatory phenotype. Conversely, chronic inflammation can induce a progesterone-resistant state. Repetitive retrograde endometrial shedding begets chronic peritoneal inflammation, which further exacerbates progesterone resistance. Genetic causes of progesterone resistance include progesterone receptor gene polymorphisms, altered microRNA expression, and epigenetic modifications to progesterone receptors and their targets. Environmental toxins such as dioxin play a possible role in the genesis of endometriosis by permitting an inflammatory milieu. A consequence of impaired progesterone action is that hormonal therapy is rendered ineffective for a subset of women with endometriosis. Synthetic progestins, such as dienogest, may overcome this phenomenon by increasing progesterone receptor expression and decreasing proinflammatory cytokines. Other modalities include high dose depot formulations of progestins, medicated intrauterine devices and the likely advent of oral GnRH antagonists. Unearthing root causes of progesterone inaction in endometriosis will aid in the development of novel therapeutics geared toward prevention and treatment.
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Alterations to decidualization contribute directly to the establishment and growth of ectopic endometrial tissue, the primary hallmark of endometriosis.
“Furthermore, these alterations to decidualization contribute directly to the establishment and growth of ectopic endometrial tissue, the primary hallmark of this disorder (Patel et al., 2017).”
From Endometriosis and polycystic ovary syndrome are diametric disorders (2021) · cites this paper as Patel et al., 2017
Local estrogen production and progesterone resistance were demonstrated in larger endometriosis lesions.
“Local estrogen production (154) and progesterone resistance (155-162) were demonstrated in larger endometriosis lesions (154-163)”
From Pathogenesis of endometriosis: The genetic/epigenetic theory (2019) · cites this paper as [162]
Some miRNAs (miR-9m, miR-34 and miR-29c) are implicated in progesterone resistance.
“some miRNAs (miR-9m, miR-34 and miR-29c) are implicated in progesterone resistance.”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [22]
In endometriotic lesions, stromal cells showing progesterone resistance are unable to produce retinoic acid, resulting in loss of 17β-HSD2 expression, failure to inactivate local E2, and high E2 activity.
“Conversely, in endometriotic lesions, stromal cells showing progesterone resistance are unable to produce RA which results in loss of 17β-HSD2 expression and failure to inactivate local E2, ultimately leading to high E2 activity [14,15,16,20,21,22].”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [22]
In endometrial stromal cells, progesterone increases formation of retinoic acid, which triggers expression of 17β-HSD2 in epithelial cells.
“In endometrial stromal cells, progesterone increases formation of RA, which triggers expression of 17β-HSD2 in epithelial cells.”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [22]
Progesterone resistance may explain non-response to estroprogestins or progestins.
“Progesterone resistance may of course explain this unexpected issue [18,19,20,21,22].”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [22]
PR deficiency is evident in endometriotic lesions, leading to progesterone resistance and defective progesterone action, with consequences on survival and development of endometriotic tissues.
“PR deficiency is evident in endometriotic lesions, leading to progesterone resistance and defective progesterone action, with obvious consequences on the survival and development of endometriotic tissues [15,22,84].”
From Endometriosis and Medical Therapy: From Progestogens to Progesterone Resistance to GnRH Antagonists: A Review (2021) · cites this paper as [22]
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- Authors
- Patel, B. G., Rudnicki, M., Yu, J., Shu, Y., & Taylor, R. N.
- Affiliations
- Wake Forest University Health Sciences (US)
- Odense University Hospital (DK)
- Corresponding author
- Rudnicki, Martin
- Venue
- Acta Obstetricia Et Gynecologica Scandinavica
- Publisher
- Wiley
- Published
- 2017-05-28
- Volume
- 96
- Issue
- 6
- Pages
- 623-632
- ISSN
- 0001-6349 (ISSN-L)
- 1600-0412
- OpenAlex
- W2605912824
- Cited by
- 336
- References
- 66
- Citations by year
- 2026: 38 · 2025: 25 · 2024: 34 · 2023: 59 · 2022: 51 · 2021: 43 · 2020: 38 · 2019: 20 · 2018: 20 · 2017: 8
- FWCI
- 3.84
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Acta Obstetricia Et Gynecologica Scandinavica (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (submittedVersion)
- Topics
- Health Sciences › Medicine › Reproductive Medicine › Endometriosis Research and Treatment
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Ectopic Pregnancy Diagnosis and Management
- Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
- Keywords
- endometriosis, progesterone resistance, progesterone signaling, decidualization, endometritis, microRNA, epigenetic modifications, dioxins, progestins, dienogest, GnRH antagonist, endocrine therapy resistance, peritonitis
- MeSH terms
- Endometriosis, Endometrium, Environmental Pollution, Female, Humans, Progesterone, Receptors, Progesterone
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