Please use this identifier to cite or link to this item: http://hdl.handle.net/10553/75027
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dc.contributor.authorLopez-Parra, Virginiaen_US
dc.contributor.authorMallavia, Beñaten_US
dc.contributor.authorLopez-Franco, Oscaren_US
dc.contributor.authorOrtiz-Muñoz, Guadalupeen_US
dc.contributor.authorOguiza, Ainhoaen_US
dc.contributor.authorRecio Cruz, Carlota Pilaren_US
dc.contributor.authorBlanco, Juliaen_US
dc.contributor.authorNimmerjahn, Falken_US
dc.contributor.authorEgido, Jesusen_US
dc.contributor.authorGómez-Guerrero, Carmenen_US
dc.date.accessioned2020-10-27T09:46:40Z-
dc.date.available2020-10-27T09:46:40Z-
dc.date.issued2012en_US
dc.identifier.issn1046-6673en_US
dc.identifier.urihttp://hdl.handle.net/10553/75027-
dc.description.abstractAmong patients with diabetes, increased production of immunoglobulins against proteins modified by diabetes is associated with proteinuria and cardiovascular risk, suggesting that immune mechanisms may contribute to the development of diabetes complications, such as nephropathy. We investigated the contribution of IgG Fcg receptors to diabetic renal injury in hyperglycemic, hypercholesterolemic mice. Weused streptozotocin to induce diabetes in apolipoprotein E–deficientmice and in mice deficient in both apolipoprotein E and g-chain, the common subunit of activating Fcg receptors. After 15 weeks, the mice lacking Fcg receptors had significantly less albuminuria and renal hypertrophy, despite similar degrees of hyperglycemia and hypercholesterolemia, immunoglobulin production, and glomerular immune deposits. Moreover, diabetic Fcg receptor–deficient mice had less mesangial matrix expansion, inflammatory cell infiltration, and collagen and a-smooth muscle actin content in their kidneys. Accordingly, expression of genes involved in leukocyte infiltration, fibrosis, and oxidative stress was significantly reduced in diabetic kidneys and in mesangial cells cultured from Fcg receptor–deficient mice. In summary, preventing the activation of Fcg receptors alleviates renal hypertrophy, inflammation, and fibrosis in hypercholesterolemic mice with diabetes, suggesting that modulating Fcg receptor signaling may be renoprotective in diabetic nephropathy.en_US
dc.languageengen_US
dc.relationSAF2009/11794en_US
dc.relationPI10/00072en_US
dc.relationRECAVA RD06/0014/0035en_US
dc.relation.ispartofJournal of the American Society of Nephrology : JASNen_US
dc.sourceJournal of the American Society of Nephrology : JASN [ISSN 1046-6673], v. 23 (9), p. 1518-1527en_US
dc.subject3207 Patologíaen_US
dc.subject320506 Nefrologíaen_US
dc.titleFcγ Receptor Deficiency Attenuates Diabetic Nephropathyen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeArticleen_US
dc.identifier.doi10.1681/ASN.2011080822en_US
dc.identifier.pmid22859852-
dc.description.lastpage1527en_US
dc.identifier.issue9-
dc.description.firstpage1518en_US
dc.relation.volume23en_US
dc.investigacionCiencias de la Saluden_US
dc.type2Artículoen_US
dc.utils.revisionen_US
dc.identifier.ulpgcNoen_US
dc.contributor.buulpgcBU-MEDen_US
dc.description.sjr5,307
dc.description.jcr8,987
dc.description.sjrqQ1
dc.description.jcrqQ1
dc.description.scieSCIE
item.fulltextCon texto completo-
item.grantfulltextopen-
crisitem.author.deptGIR IUIBS: Farmacología Molecular y Traslacional-
crisitem.author.deptIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.deptDepartamento de Ciencias Clínicas-
crisitem.author.orcid0000-0002-8832-2826-
crisitem.author.parentorgIU de Investigaciones Biomédicas y Sanitarias-
crisitem.author.fullNameRecio Cruz, Carlota Pilar-
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