Wnt Signaling in Endometriosis: Mechanisms and Therapeutic Potential

Tatiana V. Denisenko, Anna E. Ivanova, Silachev D, M R Dumanovskaya, Guzal I. Tabeeva, A. A. Smetnik, Г. Т. Сухих, Vladimir L. Katanaev
In: Medical Sciences · 2026 · vol. 14(7) , pp. 760 · doi:10.3390/medsci14070760 · W7225653424
Review OA: gold CC0
🔓 Open OA copy View on OpenAlex View at publisher

Abstract

Endometriosis is a chronic, estrogen-dependent disease that affects up to 10% of women of reproductive age and leads to pain, infertility, and impaired quality of life. Despite current hormonal and surgical therapies, many patients continue to suffer from recurrence, fibrosis, and reduced fertility, emphasizing the need for mechanism-based treatment strategies. Aberrant intracellular signaling contributes to a pathogenic network linking proliferation, inflammation, fibrotic remodeling, and therapeutic resistance. Focusing on the roles of the Wnt/β-catenin pathway, we discuss recent studies that indicate that excessive Wnt signaling may upregulate these disease-relevant cellular programs, while inhibition of the pathway may reduce the endometriotic lesion burden and fibrosis in preclinical models. Advances in Wnt-targeted therapies in oncology and fibrotic diseases now provide a timely translational framework for endometriosis. Targeting the Wnt pathway as part of broader mechanism-based therapeutic strategies may enable a shift from symptomatic treatments to non-hormonal and disease-modifying approaches.

My notes (saved in your browser only)

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (100)

Source provenance

openalex
last seen: 2026-11-11T06:04:37.277765+00:00
License: CC0 · commercial use OK