Mevalonate-Ras Homology (Rho)/Rho-Associated Coiled-Coil-Forming Protein Kinase (ROCK)-Mediated Signaling Pathway as a Therapeutic Target for the Treatment of Endometriosis-Associated Fibrosis

Kaei Nasu, Akitoshi Tsuno, Akitoshi Yuge, Hisashi Narahara
In: Current Signal Transduction Therapy · 2010 · vol. 5(2) , pp. 141–148 · doi:10.2174/157436210791112154 · W2115294908
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Endometriotic stromal cells exhibit enhanced extracellular matrix contractility and myofibroblast differentiation via the mevalonate-Rho/ROCK pathway, suggesting this pathway as a therapeutic target for endometriosis-associated fibrosis.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-16 · read from full text ⓘ

This paper reviews mechanisms of endometriosis-associated fibrosis with a focus on contractility of endometriotic stromal cells, and uses data from a three-dimensional collagen gel culture model to compare endometriotic versus normal endometrial stromal cells. The authors report that endometriotic stromal cells show enhanced extracellular matrix contractility alongside activation of the mevalonate–Rho/ROCK signaling pathway and increased myofibroblastic differentiation, consistent with collagen-driven fibrogenesis. A major caveat is that the work emphasizes mechanistic and in vitro/experimental modeling rather than clinical outcomes. This paper is centrally about endometriosis—specifically the mevalonate–Rho/ROCK-mediated signaling pathway as a therapeutic target for endometriosis-associated fibrosis.

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Abstract

Endometriosis, a disease affecting 3-10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue. Histologically, this disease is characterized by endometrial gland and stroma with surrounding dense fibrous tissue. During the development of endometriotic lesions, excess fibrosis may lead to scarring and to alteration of the tissue function. It has been suggested that type I collagen is a major contributor to endometriosis-associated fibrosis. One approach to understanding the pathogenesis of endometriosis is to investigate the mechanisms underlying fibrogenesis associated with this disease. Using three-dimensional collagen gel culture model, we have evaluated the extracellular matrix contractility and myofibroblastic differentiation of endometriotic stromal cells. Endometriotic stromal cells showed enhanced extracellular matrix contractility in comparison with normal endometrial stromal cells. Activation of the Ras homology (Rho)/Rho-associated coiled-coil-forming protein kinase (ROCK)-mediated signaling pathway with simultaneously enhanced myofibroblastic differentiation is involved in this mechanism. We have proposed the mevalonate-Rho/ROCK-mediated signaling pathways as possible therapeutic targets for the treatment of endometriosis-associated fibrosis. This paper is a review of the recent information concerning the mechanism of endometriosis-associated fibrosis, focusing on the contractility of endometriotic stromal cells. The modulators of mevalonate-Rho/ROCK signaling pathways were also evaluated as promising agents for the treatment and prevention of endometriosis-associated fibrosis. Keywords: Endometriosis, fibrosis, mevalonate-pathway, Ras homology (Rho), Rho-associated coiled-coil-forming protein kinase
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Abstract

Endometriosis, a disease affecting 3-10% of women of reproductive age, is characterized by the ectopic growth of endometrial tissue. Histologically, this disease is characterized by endometrial gland and stroma with surrounding dense fibrous tissue. During the development of endometriotic lesions, excess fibrosis may lead to scarring and to alteration of the tissue function. It has been suggested that type I collagen is a major contributor to endometriosis-associated fibrosis. One approach to understanding the pathogenesis of endometriosis is to investigate the mechanisms underlying fibrogenesis associated with this disease. Using three-dimensional collagen gel culture model, we have evaluated the extracellular matrix contractility and myofibroblastic differentiation of endometriotic stromal cells. Endometriotic stromal cells showed enhanced extracellular matrix contractility in comparison with normal endometrial stromal cells. Activation of the Ras homology (Rho)/Rho-associated coiled-coil-forming protein kinase (ROCK)-mediated signaling pathway with simultaneously enhanced myofibroblastic differentiation is involved in this mechanism. We have proposed the mevalonate-Rho/ROCK-mediated signaling pathways as possible therapeutic targets for the treatment of endometriosis-associated fibrosis. This paper is a review of the recent information concerning the mechanism of endometriosis-associated fibrosis, focusing on the contractility of endometriotic stromal cells. The modulators of mevalonate-Rho/ROCK signaling pathways were also evaluated as promising agents for the treatment and prevention of endometriosis-associated fibrosis.

Keywords

Endometriosis, fibrosis, mevalonate-pathway, Ras homology (Rho), Rho-associated coiled-coil-forming protein kinase 4

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