Additional file 1 of Activation of α7 nicotinic acetylcholine receptor retards the development of endometriosis
This study evaluated the number of endometriotic lesions in mice treated with PNU-282987, demonstrating that activation of the α7 nicotinic acetylcholine receptor retards endometriosis development.
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References (54)
- Alpha-7 nicotinic acetylcholine receptor (nAChR) agonist inhibits the development of endometriosis by regulating inflammation via openalex
- Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious via openalex
- Cellular Changes Consistent With Epithelial-Mesenchymal Transition and Fibroblast-to-Myofibroblast Transdifferentiation in the Progression of Experimental Endometriosis in Baboons via openalex
- Chronic stress accelerates the development of endometriosis in mouse through adrenergic receptor β2 via openalex
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- Endometriosis: pathogenesis and treatment via openalex
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- Management of endometriomas in women requiring IVF: to touch or not to touch via openalex
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- Platelets drive smooth muscle metaplasia and fibrogenesis in endometriosis through epithelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation via openalex
- Platelets induce endothelial-mesenchymal transition and subsequent fibrogenesis in endometriosis via openalex
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- Trichostatin A, a histone deacetylase inhibitor, reduces lesion growth and hyperalgesia in experimentally induced endometriosis in mice via openalex
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