Please use this identifier to cite or link to this item: http://ricaxcan.uaz.edu.mx/jspui/handle/20.500.11845/1497
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dc.contributor49237es_ES
dc.contributor268446es_ES
dc.contributor.otherhttps://orcid.org/0000-0002-7635-4687-
dc.coverage.spatialGlobales_ES
dc.creatorMartínez Fierro, Margarita de la Luz-
dc.creatorHernández Delgadillo, Gloria Patricia-
dc.creatorFlores Morales, Virginia-
dc.creatorCardenas Vargas, Edith-
dc.creatorMercado Reyes, Marisa-
dc.creatorRodríguez Sánchez, Iram Pablo-
dc.creatorDelgado Enciso, Iván-
dc.creatorGalván Tejada, Carlos Eric-
dc.creatorGalván Tejada, Jorge Issac-
dc.creatorCelaya Padilla, José María-
dc.creatorGarza Veloz, Idalia-
dc.date.accessioned2020-04-08T18:51:01Z-
dc.date.available2020-04-08T18:51:01Z-
dc.date.issued2018-02-07-
dc.identifierinfo:eu-repo/semantics/publishedVersiones_ES
dc.identifier.issn1535-3702es_ES
dc.identifier.urihttp://ricaxcan.uaz.edu.mx/jspui/handle/20.500.11845/1497-
dc.identifier.urihttps://doi.org/10.48779/cr4f-hj09-
dc.description.abstractPreeclampsia (PE) is a pregnancy complex disease, distinguished by high blood pressure and proteinuria, diagnosed after the 20th gestation week. Depending on the values of blood pressure, urine protein concentrations, symptomatology, and onset of disease there is a wide range of phenotypes, from mild forms developing predominantly at the end of pregnancy to severe forms developing in the early stage of pregnancy. In the worst cases severe forms of PE could lead to systemic endothelial dysfunction, eclampsia, and maternal and/or fetal death. Worldwide the fetal morbidity and mortality related to PE is calculated to be around 8% of the total pregnancies. PE still being an enigma regarding its etiology and pathophysiology, in general a deficient trophoblast invasion during placentation at first stage of pregnancy, in combination with maternal conditions are accepted as a cause of endothelial dysfunction, inflammatory alterations and appearance of symptoms. Depending on the PE multifactorial origin, several in vitro, in vivo,andin silico models have been used to evaluate the PE pathophysiology as well as to identify or test biomarkers predicting, diagnosing or prognosing the syndrome. This review focuses on the most common models used for the study of PE, including those related to placental development, abnormal trophoblast invasion, uteroplacental ischemia, angiogenesis, oxygen deregulation, and immune response to maternal–fetal interactions. The advances in mathematical and computational modeling of metabolic network behavior, gene prioritization, the protein–protein interaction network, the genetics of PE, and the PE prediction/classification are discussed. Finally, the potential of these models to enable understanding of PE pathogenesis and to evaluate new preventative and therapeutic approaches in the management of PE are also highlighted.es_ES
dc.language.isoenges_ES
dc.publisherSAGE Journalses_ES
dc.relationhttps://journals.sagepub.com/doi/abs/10.1177/1535370218755690es_ES
dc.relation.urigeneralPublices_ES
dc.rightsAtribución-NoComercial-CompartirIgual 3.0 Estados Unidos de América*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/us/*
dc.sourceExperimental Biology and Medicine Vol 243, No. 6, pp. 1-10es_ES
dc.subject.classificationINGENIERIA Y TECNOLOGIA [7]es_ES
dc.subject.otherpreeclampsiaes_ES
dc.subject.otherModel systemses_ES
dc.subject.otherstudyes_ES
dc.titleCurrent model systems for the study of preeclampsiaes_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
Appears in Collections:*Documentos Académicos*-- Doc. en Ing. y Tec. Aplicada

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