Fasudil inhibits the proliferation and contractility and induces cell cycle arrest and apoptosis of human endometriotic stromal cells: a promising agent for the treatment of endometriosis

Tsuno A, Akitoshi Tsuno, Nasu K, Kaei Nasu, Yukie Kawano, Kawano Y, Yuge A, Akitoshi Yuge, Li H, Haili Li, Wakana Abe, Abe W, Narahara H, Hisashi Narahara
The Journal of clinical endocrinology and metabolism · 2011 · vol. 96(12) , pp. E1944–E1952 · doi:10.1210/jc.2011-1503 · PMID:21917869 · W2011463618
Lab / animal OA: hybrid CC0 ⤵ 14 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-08 ⓘ

Fasudil, a ROCK inhibitor, decreased human endometriotic stromal cell proliferation and contractility while inducing cell cycle arrest and apoptosis, suggesting it may be a treatment for endometriosis.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

CONTEXT: During the development of endometriotic lesions, excess fibrosis may lead to scarring and to the alterations of tissue function that are the characteristic features of this disease. Enhanced extracellular matrix contractility of endometriotic stromal cells (ECSC) mediated by the mevalonate-Ras homology (Rho)/Rho-associated coiled-coil-forming protein kinase (ROCK) pathway has been shown to contribute to the pathogenesis of endometriosis. DESIGN: To assess the use of fasudil, a selective ROCK inhibitor, for the medical treatment of endometriosis-associated fibrosis, the effects of this agent on the cell proliferation, apoptosis, cell cycle, morphology, cell density, and contractility of ECSC were investigated. The effects of fasudil on the expression of contractility-related, apoptosis-related, and cell cycle-related molecules in ECSC were also evaluated. RESULTS: Fasudil significantly inhibited the proliferation and contractility of ECSC and induced the cell cycle arrest in the G2/M phase and apoptosis of these cells. Morphological observation revealed the suppression of ECSC attachment to collagen fibers and decrease of cell density by fasudil. The expression of α-smooth muscle actin, RhoA, ROCK-I, and ROCK-II proteins was inhibited by fasudil administration. The expression of the antiapoptotic factors, Bcl-2 and Bcl-X(L), in two-dimensional cultured ECSC were down-regulated by the addition of fasudil, whereas, the expression of p16(INK4a) and p21(Waf1/Cip1) was up-regulated by the addition of fasudil. CONCLUSIONS: The present findings suggest that fasudil is a promising agent for the treatment of endometriosis. The inhibition of cell proliferation, contractility, and myofibroblastic differentiation, the attenuation of attachment to collagen fibers, the decrease of cell density, and the induction of cell cycle arrest and apoptosis of ECSC are involved in the active mechanisms of fasudil.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine Apoptosis Cell Cycle Cell Proliferation Endometriosis Ovarian Diseases Protein Kinase Inhibitors Stromal Cells 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine Adult Adult Apoptosis Apoptosis Cell Cycle Cell Cycle Cell Proliferation Cell Proliferation Endometriosis

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 (42)

Cited by (15)

Source provenance

europepmc
last seen: 2026-10-13T06:10:10.580696+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:09:27.188120+00:00
License: CC0 · commercial use OK