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dc.contributor.authorNicoletto, Bruna Bellincantapt_BR
dc.contributor.authorCanani, Luis Henrique Santospt_BR
dc.date.accessioned2020-01-30T04:09:13Zpt_BR
dc.date.issued2015pt_BR
dc.identifier.issn1758-5996pt_BR
dc.identifier.urihttp://hdl.handle.net/10183/205070pt_BR
dc.description.abstractProgranulin (PGRN) is a cysteine rich secreted protein, expressed in epithelial cells, immune cells, neurons, and adipocytes. It was first identified for its growth factor-like properties, being involved in early embryogenesis and tissue remodeling, acting as an anti-inflammatory molecule. In the central nervous system, PGRN has neurotrophic and neuroprotective actions. There is also evidence of PGRN effects on cancer, contributing to tumor proliferation, invasion and cell survival. Recently, PGRN was recognized as an adipokine related to obesity and insulin resistance, revealing its metabolic function and pro-inflammatory properties. In obesity and type 2 diabetes mellitus, PGRN levels are increased. In renal disease, there is a relevant association, however, it is not known if it could contribute to kidney damage or if it is only a route of PGRN elimination. PGRN is an emerging molecule which demands studies in different fields. Possibly, it plays distinct functions in different tissues/cells and metabolic conditions. Here, we discuss potential mechanisms and recent data of PGRN pro-inflammatory actions, regarding obesity, insulin resistance, type 2 diabetes mellitus and kidney disease.en
dc.format.mimetypeapplication/pdfpt_BR
dc.language.isoengpt_BR
dc.relation.ispartofDiabetology & metabolic syndrome. São Paulo. Vol. 7:117 (2015), 8 p.pt_BR
dc.rightsOpen Accessen
dc.subjectProgranulinen
dc.subjectAdipocinaspt_BR
dc.subjectAdipokineen
dc.subjectNefritept_BR
dc.subjectObesidadept_BR
dc.subjectObesityen
dc.subjectDiabetesen
dc.subjectKidney diseaseen
dc.subjectInflammationen
dc.titleThe role of progranulin in diabetes and kidney diseasept_BR
dc.typeArtigo de periódicopt_BR
dc.identifier.nrb001000450pt_BR
dc.type.originNacionalpt_BR


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