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Progress in Establishment of Endometriosis in Vitro Histological Models
Science Discovery
Volume 6, Issue 6, December 2018, Pages: 551-554
Received: Dec. 26, 2018; Published: Dec. 27, 2018
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Ma Di, Obstetrics and Gynecology Department, First Affiliated Hospital of Harbin Medical University, Harbin, China
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The etiology and pathogenesis of endometriosis are hotspots in the field of obstetrics and gynecology today.With the rapid development of experimental studies of endometriosis, the establishment of in vitro histological models is increasingly important.The establishment and application of in vitro histological model provides a new research platform for exploring the pathogenesis and treatment of endometriosis. It is an important method to study endometriosis. Recently a variety of models have been successfully constructed, but still have many deficiencies. Up to now, studies on in vitro histological models have been qualitative, and no studies have involved quantitative analysis. Whether peritoneal mesothelial defect is the cause or result of adhesion, that is, peritoneal mesothelial defect itself exists in the patient, or the damage of the mesothelial during operation, or the destruction of the mesothelial by some cytokines secreted by implanted endometrial tissue? These problems have not yet been decided. Therefore, the choice of appropriate histological model to establish a method is conducive to further reveal the etiology of endometriosis, pathogenesis and evaluation of treatment. This paper reviews the research progress about the development of endometriosis with establishment of in vitro histological models, to further explore the best and stable culture conditions of human endometriosis histological model, and to establish a good model basis for further study of endometriosis.
Endometriosis, Establishment of Vitro Histological Models, Research Progress
To cite this article
Ma Di, Progress in Establishment of Endometriosis in Vitro Histological Models, Science Discovery. Vol. 6, No. 6, 2018, pp. 551-554. doi: 10.11648/
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