FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2078993601> ?p ?o ?g. }

• W2078993601 endingPage "e418" @default.
• W2078993601 startingPage "e418" @default.
• W2078993601 abstract "A resolutive therapy for Duchene muscular dystrophy, a severe degenerative disease of the skeletal muscle, is still lacking. Because autophagy has been shown to be crucial in clearing dysfunctional organelles and in preventing tissue damage, we investigated its pathogenic role and its suitability as a target for new therapeutic interventions in Duchenne muscular dystrophy (DMD). Here we demonstrate that autophagy is severely impaired in muscles from patients affected by DMD and mdx mice, a model of the disease, with accumulation of damaged organelles. The defect in autophagy was accompanied by persistent activation via phosphorylation of Akt, mammalian target of rapamycin (mTOR) and of the autophagy-inhibiting pathways dependent on them, including the translation-initiation factor 4E-binding protein 1 and the ribosomal protein S6, and downregulation of the autophagy-inducing genes LC3, Atg12, Gabarapl1 and Bnip3. The defective autophagy was rescued in mdx mice by long-term exposure to a low-protein diet. The treatment led to normalisation of Akt and mTOR signalling; it also reduced significantly muscle inflammation, fibrosis and myofibre damage, leading to recovery of muscle function. This study highlights novel pathogenic aspects of DMD and suggests autophagy as a new effective therapeutic target. The treatment we propose can be safely applied and immediately tested for efficacy in humans." @default.
• W2078993601 created "2016-06-24" @default.
• W2078993601 creator A5001395158 @default.
• W2078993601 creator A5010848776 @default.
• W2078993601 creator A5028331696 @default.
• W2078993601 creator A5052576774 @default.
• W2078993601 creator A5062671029 @default.
• W2078993601 creator A5063374823 @default.
• W2078993601 creator A5077743857 @default.
• W2078993601 creator A5078196954 @default.
• W2078993601 creator A5079925252 @default.
• W2078993601 creator A5086637902 @default.
• W2078993601 creator A5087520444 @default.
• W2078993601 creator A5089112768 @default.
• W2078993601 date "2012-11-15" @default.
• W2078993601 modified "2023-10-07" @default.
• W2078993601 title "Autophagy as a new therapeutic target in Duchenne muscular dystrophy" @default.
• W2078993601 cites W1514670900 @default.
• W2078993601 cites W1586159393 @default.
• W2078993601 cites W166700135 @default.
• W2078993601 cites W1964167542 @default.
• W2078993601 cites W1977964721 @default.
• W2078993601 cites W1978967566 @default.
• W2078993601 cites W1985183676 @default.
• W2078993601 cites W2007790958 @default.
• W2078993601 cites W2013648458 @default.
• W2078993601 cites W2015870495 @default.
• W2078993601 cites W2016040396 @default.
• W2078993601 cites W2018567399 @default.
• W2078993601 cites W2025192214 @default.
• W2078993601 cites W2034132952 @default.
• W2078993601 cites W2035555824 @default.
• W2078993601 cites W2035637866 @default.
• W2078993601 cites W2036132575 @default.
• W2078993601 cites W2036787961 @default.
• W2078993601 cites W2039306818 @default.
• W2078993601 cites W2040533720 @default.
• W2078993601 cites W2040691328 @default.
• W2078993601 cites W2054189227 @default.
• W2078993601 cites W2058425371 @default.
• W2078993601 cites W2061394006 @default.
• W2078993601 cites W2064576222 @default.
• W2078993601 cites W2080417224 @default.
• W2078993601 cites W2081872244 @default.
• W2078993601 cites W2086072733 @default.
• W2078993601 cites W2103545941 @default.
• W2078993601 cites W2103597137 @default.
• W2078993601 cites W2107045511 @default.
• W2078993601 cites W2115742671 @default.
• W2078993601 cites W2117224856 @default.
• W2078993601 cites W2119399459 @default.
• W2078993601 cites W2125564749 @default.
• W2078993601 cites W2128677681 @default.
• W2078993601 cites W2131396113 @default.
• W2078993601 cites W2135574023 @default.
• W2078993601 cites W2136000647 @default.
• W2078993601 cites W2139162336 @default.
• W2078993601 cites W2154041187 @default.
• W2078993601 cites W2159796957 @default.
• W2078993601 cites W2163958066 @default.
• W2078993601 cites W2164316354 @default.
• W2078993601 cites W2164343307 @default.
• W2078993601 cites W2168107233 @default.
• W2078993601 cites W2169836157 @default.
• W2078993601 cites W4238163958 @default.
• W2078993601 doi "https://doi.org/10.1038/cddis.2012.159" @default.
• W2078993601 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4454298" @default.
• W2078993601 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25101676" @default.
• W2078993601 hasPublicationYear "2012" @default.
• W2078993601 type Work @default.
• W2078993601 sameAs 2078993601 @default.
• W2078993601 citedByCount "194" @default.
• W2078993601 countsByYear W20789936012013 @default.
• W2078993601 countsByYear W20789936012014 @default.
• W2078993601 countsByYear W20789936012015 @default.
• W2078993601 countsByYear W20789936012016 @default.
• W2078993601 countsByYear W20789936012017 @default.
• W2078993601 countsByYear W20789936012018 @default.
• W2078993601 countsByYear W20789936012019 @default.
• W2078993601 countsByYear W20789936012020 @default.
• W2078993601 countsByYear W20789936012021 @default.
• W2078993601 countsByYear W20789936012022 @default.
• W2078993601 countsByYear W20789936012023 @default.
• W2078993601 crossrefType "journal-article" @default.
• W2078993601 hasAuthorship W2078993601A5001395158 @default.
• W2078993601 hasAuthorship W2078993601A5010848776 @default.
• W2078993601 hasAuthorship W2078993601A5028331696 @default.
• W2078993601 hasAuthorship W2078993601A5052576774 @default.
• W2078993601 hasAuthorship W2078993601A5062671029 @default.
• W2078993601 hasAuthorship W2078993601A5063374823 @default.
• W2078993601 hasAuthorship W2078993601A5077743857 @default.
• W2078993601 hasAuthorship W2078993601A5078196954 @default.
• W2078993601 hasAuthorship W2078993601A5079925252 @default.
• W2078993601 hasAuthorship W2078993601A5086637902 @default.
• W2078993601 hasAuthorship W2078993601A5087520444 @default.
• W2078993601 hasAuthorship W2078993601A5089112768 @default.
• W2078993601 hasBestOaLocation W20789936011 @default.
• W2078993601 hasConcept C104202773 @default.

• next