| http://purl.uniprot.org/citations/24163134 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/24163134 | http://www.w3.org/2000/01/rdf-schema#comment | "Duchenne muscular dystrophy (DMD) is the most common inherited neuromuscular disease, and is characterized by the lack of dystrophin, muscle wasting, increased transforming growth factor (TGF)-β Smad-dependent signalling and fibrosis. Acting via the Mas receptor, angiotensin-1-7 [Ang-(1-7)], is part of the renin-angiotensin system, with the opposite effect to that of angiotensin II. We hypothesized that the Ang-(1-7)/Mas receptor axis might protect chronically damaged tissues as in skeletal muscle of the DMD mouse model mdx. Infusion or oral administration of Ang-(1-7) in mdx mice normalized skeletal muscle architecture, decreased local fibrosis and improved muscle function in vitro and in vivo. These positive effects were mediated by the inhibition of TGF-β Smad signalling, which in turn led to reduction of the pro-fibrotic microRNA miR-21 concomitant with a reduction in the number of TCF4 expressing fibroblasts. Mdx mice infused with Mas antagonist (A-779) and mdx deficient for the Mas receptor showed highly deteriorated muscular architecture, increased fibrosis and TGF-β signalling with diminished muscle strength. These results suggest that this novel compound Ang-(1-7) might be used to improve quality of life and delay death in individuals with DMD and this drug should be investigated in further pre-clinical trials."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.org/dc/terms/identifier | "doi:10.1093/hmg/ddt514"xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Bader M."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Munoz-Canoves P."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Santos R.A."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Cabrera D."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Brandan E."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Olguin H."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Vio C.P."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Cabello-Verrugio C."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Pessina P."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/author | "Acuna M.J."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/date | "2014"xsd:gYear |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/name | "Hum Mol Genet"xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/pages | "1237-1249"xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/title | "Restoration of muscle strength in dystrophic muscle by angiotensin-1-7 through inhibition of TGF-beta signalling."xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://purl.uniprot.org/core/volume | "23"xsd:string |
| http://purl.uniprot.org/citations/24163134 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/24163134 |
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