# Signaling pathways and advances in targeted therapy for adenomyosis

**Authors:** Yue Li, Hongyu Zhang, Yaoyao Ding, Yiling Zhao, Yufeng Li, Tiansheng Qin

PMC · DOI: 10.3389/fcell.2025.1685525 · Frontiers in Cell and Developmental Biology · 2025-11-06

## TL;DR

This review explores signaling pathways involved in adenomyosis and highlights new targeted therapies to improve treatment options.

## Contribution

The paper provides a comprehensive overview of signaling pathways and emerging targeted therapies for adenomyosis.

## Key findings

- Adenomyosis involves dysregulation of multiple signaling pathways like VEGF, Wnt, and PI3K.
- Emerging therapies include multi-target combination treatments and epigenetic regulation.
- Natural products are highlighted as potential future treatment options for adenomyosis.

## Abstract

Adenomyosis is a common estrogen-dependent disease, characterized by the invasion of endometrial glands and stroma into the myometrium. It often results in dysmenorrhea, menorrhagia, and infertility, significantly impacting patients’ quality of life. Currently, the etiology and pathogenesis of adenomyosis remain unclear, and existing treatments have limitations. Therefore, further research on the mechanism and treatment of adenomyosis is urgently needed. Studies indicate that adenomyosis involves dysregulation of multiple signaling pathways, including VEGF, Wnt, PI3K, MAPK, NF-κB, cGAS-STING, TGF-β, Hedgehog, and Hippo pathways, which regulate processes such as estrogen and progesterone imbalance, angiogenesis, proliferation and invasion, and the processes of inflammation and fibrosis. This review summarizes the relevant signaling pathways involved in adenomyosis and discusses recent progress in targeted pathway therapies. Additionally, emerging therapeutic strategies such as multi-target combination therapy, epigenetic regulation, and natural products are emphasized as viable avenues for adenomyosis treatment in the future.

## Linked entities

- **Diseases:** adenomyosis (MONDO:0010888)

## Full-text entities

- **Genes:** CGAS (cyclic GMP-AMP synthase) [NCBI Gene 115004] {aka C6orf150, D4, MB21D1, h-cGAS}, PIK3CB (phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta) [NCBI Gene 5291] {aka P110BETA, PI3K, PI3KBETA, PIK3C1}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, NFKB1 (nuclear factor kappa B subunit 1) [NCBI Gene 4790] {aka CVID12, EBP-1, KBF1, NF-kB, NF-kB1, NF-kappa-B1}, STING1 (stimulator of interferon response cGAMP interactor 1) [NCBI Gene 340061] {aka ERIS, MITA, MPYS, NET23, SAVI, STING}
- **Diseases:** dysmenorrhea (MESH:D004412), infertility (MESH:D007246), Adenomyosis (MESH:D062788), fibrosis (MESH:D005355), estrogen-dependent (MESH:D056828), menorrhagia (MESH:D008595), inflammation (MESH:D007249)
- **Chemicals:** progesterone (MESH:D011374)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12635047/full.md

## References

81 references — full list in the complete paper: https://tomesphere.com/paper/PMC12635047/full.md

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Source: https://tomesphere.com/paper/PMC12635047