Molecular Mechanisms Underlying the Link between Nuclear Receptor Function and Cholesterol Gallstone Formation

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dc.contributor.authorVazquez, M. C.
dc.contributor.authorRigotti Rivera, Attilio
dc.contributor.authorZanlungo Matsuhiro, Silvana
dc.date.accessioned2020-01-12T03:51:27Z
dc.date.available2020-01-12T03:51:27Z
dc.date.issued2012
dc.description.abstractCholesterol gallstone disease is highly prevalent in western countries, particularly in women and some specific ethnic groups. The formation of water-insoluble cholesterol crystals is due to a misbalance between the three major lipids present in the bile: cholesterol, bile salts, and phospholipids. Many proteins implicated in biliary lipid secretion in the liver are regulated by several transcription factors, including nuclear receptors LXR and FXR. Human and murine genetic, physiological, pathophysiological, and pharmacological evidence is consistent with the relevance of these nuclear receptors in gallstone formation. In addition, there is emerging data that also suggests a role for estrogen receptor ESR1 in abnormal cholesterol metabolism leading to gallstone disease. A better comprehension of the role of nuclear receptor function in gallstone formation may help to design new and more effective therapeutic strategies for this highly prevalent disease condition.
dc.fuente.origenFacultad de Medicina
dc.identifier.doi10.1155/2012/547643
dc.identifier.issn2090-3049
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/27408
dc.identifier.urihttps://doi.org/10.1155/2012/547643
dc.language.isoen
dc.nota.accesocontenido completo
dc.pagina.final7
dc.pagina.inicio1
dc.revistaJournal of Lipids
dc.rightsacceso abierto
dc.subject.ddc610
dc.subject.deweyMedicina y saludes_ES
dc.subject.ods03 Good health and well-being
dc.subject.odspa03 Salud y bienestar
dc.subject.otherCálculos biliareses_ES
dc.subject.otherColesteroles_ES
dc.subject.otherLípidoses_ES
dc.titleMolecular Mechanisms Underlying the Link between Nuclear Receptor Function and Cholesterol Gallstone Formationes_ES
dc.typeartículo
dc.volumenVol. 2012
sipa.codpersvinculados68489
sipa.codpersvinculados72650
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