Simvastatin inhibits the proliferation and the contractility of human endometriotic stromal cells: a promising agent for the treatment of endometriosis
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Simvastatin was investigated for its effects on human endometriotic stromal cells, revealing its capacity to inhibit both cell proliferation and contractility.
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Abstract
Simvastatin significantly inhibited the proliferation of endometriotic stromal cells, attenuated the collagen gel contraction mediated by these cells, and suppressed endometriotic stromal cell attachment to collagen fibers. Simvastatin is considered to be a promising agent for the treatment of endometriosis-associated fibrosis, which is among the major pathologies caused by endometriosis.
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- Medical management of endometriosis: emerging evidence linking inflammation to disease pathophysiology. 2013
- Effects of Simvastatin on Retinoic Acid System in Primary Human Endometrial Stromal Cells and in a Chimeric Model of Human Endometriosis 2013
- Simvastatin Decreases Invasiveness of Human Endometrial Stromal Cells1 2012
- Statins Inhibit Monocyte Chemotactic Protein 1 Expression in Endometriosis 2012
- Novel Therapies Targeting Endometriosis 2011
- 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 2011
- 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 2010
- Simvastatin Induces Apoptosis and Alters Cytoskeleton in Endometrial Stromal Cells 2010
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