Missing links in preeclampsia cell model systems of endothelial dysfunction

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dc.contributor.authorViana-Mattioli, Sarah [UNESP]
dc.contributor.authorFonseca-Alaniz, Miriam Helena
dc.contributor.authorPinheiro-de-Sousa, Iguaracy
dc.contributor.authorKrieger, José Eduardo
dc.contributor.authorSandrim, Valéria Cristina [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (UNESP)
dc.contributor.institutionUniversidade de São Paulo (USP)
dc.contributor.institutionEuropean Bioinformatics Institute
dc.date.accessioned2023-07-29T14:01:46Z
dc.date.available2023-07-29T14:01:46Z
dc.date.issued2023-07-01
dc.description.abstractPreeclampsia, one of the main hypertensive disorders of pregnancy, is associated with circulating factors released by the ischemic placenta accompanied by systemic endothelial dysfunction. The etiology of preeclampsia remains poorly understood although it is associated with high maternal and fetal mortality and increased cardiovascular disease risk. Most cell model systems used for studying endothelial dysfunction have not taken into account hemodynamic physical factors such as shear-stress forces which may prevent extrapolation of cell data to in vivo settings. We overview the role of hemodynamic forces in modulating endothelial cell function and discuss strategies to reproduce this biological characteristic in vitro to improve our understanding of endothelial dysfunction associated with preeclampsia.en
dc.description.affiliationDepartment of Biophysics and Pharmacology Institute of Biosciences Sao Paulo State University (UNESP), São Paulo
dc.description.affiliationLaboratory of Genetics and Molecular Cardiology Heart Institute (InCor) University of Sao Paulo Medical School, São Paulo
dc.description.affiliationEuropean Molecular Biology Laboratory European Bioinformatics Institute
dc.description.affiliationUnespDepartment of Biophysics and Pharmacology Institute of Biosciences Sao Paulo State University (UNESP), São Paulo
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipIdFAPESP: 2019/07230-8
dc.description.sponsorshipIdFAPESP: 2021/12010-7
dc.description.sponsorshipIdCNPq: 308504/2021-6
dc.description.sponsorshipIdCNPq: 408426/2021-7
dc.description.sponsorshipIdCAPES: 88887.604855/2021-00
dc.format.extent541-553
dc.identifierhttp://dx.doi.org/10.1016/j.molmed.2023.04.003
dc.identifier.citationTrends in Molecular Medicine, v. 29, n. 7, p. 541-553, 2023.
dc.identifier.doi10.1016/j.molmed.2023.04.003
dc.identifier.issn1471-499X
dc.identifier.issn1471-4914
dc.identifier.scopus2-s2.0-85159085520
dc.identifier.urihttp://hdl.handle.net/11449/249076
dc.language.isoeng
dc.relation.ispartofTrends in Molecular Medicine
dc.sourceScopus
dc.subjectendothelial dysfunction
dc.subjectomics
dc.subjectpreeclampsia
dc.subjectshear stress
dc.titleMissing links in preeclampsia cell model systems of endothelial dysfunctionen
dc.typeResenha
unesp.author.orcid0000-0002-6168-7470[5]

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