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dc.contributor.authorAsghari, S
dc.contributor.authorValizadeh, A
dc.contributor.authorAghebati-Maleki, L
dc.contributor.authorNouri, M
dc.contributor.authorYousefi, M
dc.date.accessioned2018-08-26T04:52:45Z
dc.date.available2018-08-26T04:52:45Z
dc.date.issued2018
dc.identifier.urihttp://dspace.tbzmed.ac.ir:8080/xmlui/handle/123456789/37673
dc.description.abstractEndometriosis refers to the growth of ectopic endometrial tissue outside the uterine cavity. About 10-15% of female in reproductive age suffer from endometriosis. Several etiologies - such as oxidative stress, inflammatory factors and cytokines, genetic etiology, and hormone role - have been reported for endometriosis. Indeed, oxidative stress leads to abnormalities by the production of ROS and RNS. The mechanism of endometriosis genesis is a complicated process that concerns the alterations in cellular immunity. Also, endometriosis is a hormonal response that illustrates stimulation in steroid hormone production. Genetic polymolymorphisms and epigenetic factors are also important in endometriosis initiation and progression. This review paper presents the role of oxidative stress, reactive oxygen species (ROS), and antioxidants and inflammatory, genetic, and epigenetic factors involved in the initiation and progression of the endometriosis.
dc.language.isoEnglish
dc.relation.ispartofBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
dc.titleEndometriosis: Perspective, lights, and shadows of etiology.
dc.typearticle
dc.citation.volume106
dc.citation.spage163
dc.citation.epage174
dc.citation.indexPubmed
dc.identifier.DOIhttps://doi.org/10.1016/j.biopha.2018.06.109


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