Phosphatidylinositol-3 kinase-Akt-mammalian target of rapamycin signaling pathway mediates contractility of human endometriotic stromal cells: A promising new target for the treatment of endometriosis-associated fibrosis

Wakana Abe, Kaei Nasu, Akitoshi Tsuno, Yukie Kawano, Hisashi Narahara
In: Gynecology and Minimally Invasive Therapy · 2014 · vol. 3(4) , pp. 115–118 · doi:10.1016/j.gmit.2014.07.001 · W2083496595
Lab / animal OA: diamond CC0 ⤵ 6 in-corpus citations
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This study found that inhibiting the PI3K-Akt-mTOR signaling pathway reduced the contractility of human endometriotic stromal cells in vitro, suggesting this pathway's role in endometriosis-associated fibrosis.

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Abstract

Objective: To assess the involvement of phosphatidylinositol-3 kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) on the extracellular matrix contractility of endometriotic cells. Materials and methods: The effects of wortmannin, LY294002, Akt inhibitor IV, and Ku-0063794 on the contractility of endometriotic cyst stromal cells (ECSCs) were investigated using collagen gel contraction assay. Results: All four inhibitors of PI3K-Akt-mTOR evaluated in the current study significantly inhibited the contractility of ECSCs. Conclusion: The current findings suggest that the PI3K-Akt-mTOR signaling pathway is involved in the development of endometriosis-associated fibrosis. The PI3K-Akt-mTOR signaling pathway is a promising target for the treatment of endometriosis.

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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 ]

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