English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/150828
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:


NOD1 activation in cardiac fibroblasts induces myocardial fibrosis in a murine model of type 2 diabetes

AuthorsVal-Blasco, Almudena; Prieto, Patricia ; González-Ramos, Silvia; Benito, Gemma; González-Peramato, Pilar; Agra, Noelia ; Terrón, Verónica ; Delgado, Carmen ; Martín-Sanz, Paloma ; Boscá, Lisardo ; Fernández-Velasco, María
Issue Date2017
PublisherPortland Press
Biochemical Society
CitationBiochemical Journal 474(3): 399-410 (2017)
AbstractCardiac fibrosis and chronic inflammation are common complications in type 2 diabetes mellitus (T2D). Since nucleotide oligomerization-binding domain 1 (NOD1), an innate immune receptor, is involved in the pathogenesis of insulin resistance and diabetes outcomes, we sought to investigate its involvement in cardiac fibrosis. Here, we show that selective staining of cardiac fibroblasts from T2D (db/db;db) mice exhibits up-regulation and activation of the NOD1 pathway, resulting in enhanced NF-κB and TGF-β signalling. Activation of the TGF-β pathway in cardiac fibroblasts from db mice was prevented after inhibition of NF-κB with BAY-11-7082 (BAY). Moreover, fibrosis progression in db mice was also prevented by BAY treatment. Enhanced TGF-β signalling and cardiac fibrosis of db mice was dependent, at least in part, on the sequential activation of NOD1 and NF-κB since treatment of db mice with a selective NOD1 agonist induced activation of the TGF-β pathway, but co-administration of a NOD1 agonist plus BAY, or a NOD1 inhibitor prevented the NOD1-induced fibrosis. Therefore, NOD1 is involved in cardiac fibrosis associated with diabetes, and establishes a new mechanism for the development of heart fibrosis linked to T2D.
Identifiersdoi: 10.1042/BCJ20160556
e-issn: 1470-8728
issn: 0264-6021
Appears in Collections:(IIBM) Artículos
Files in This Item:
File Description SizeFormat 
accesoRestringido.pdf15,38 kBAdobe PDFThumbnail
Show full item record
Review this work

Related articles:

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.