FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2137106285> ?p ?o ?g. }

• W2137106285 endingPage "772" @default.
• W2137106285 startingPage "763" @default.
• W2137106285 abstract "Activation of Janus kinase/signal transducers and activators of transcription (JAK/STAT) is an important mechanism by which hyperglycemia contributes to renal damage, suggesting that modulation of this pathway may prevent renal and vascular complications of diabetes. Here, we investigated the involvement of suppressors of cytokine signaling (SOCS) as intracellular negative regulators of JAK/STAT activation in diabetic nephropathy. In a rat model, inducing diabetes resulted in JAK/STAT activation and increased expression of SOCS1 and SOCS3. In humans, we observed increased expression of glomerular and tubulointerstitial SOCS proteins in biopsies of patients with diabetic nephropathy. In vitro, high concentrations of glucose activated JAK/STAT/SOCS in human mesangial and tubular cells. Overexpression of SOCS reversed the glucose-induced activation of the JAK/STAT pathway, expression of STAT-dependent genes (chemokines, growth factors, and extracellular matrix proteins), and cell proliferation. In vivo, intrarenal delivery of adenovirus expressing SOCS1 and SOCS3 to diabetic rats significantly improved renal function and reduced renal lesions associated with diabetes, such as mesangial expansion, fibrosis, and influx of macrophages. SOCS gene delivery also decreased the activation of STAT1 and STAT3 and the expression of proinflammatory and profibrotic proteins in the diabetic kidney. In summary, these results provide direct evidence for a link between the JAK/STAT/SOCS axis and hyperglycemia-induced cell responses in the kidney. Suppression of the JAK/STAT pathway by increasing intracellular SOCS proteins may have therapeutic potential in diabetic nephropathy." @default.
• W2137106285 created "2016-06-24" @default.
• W2137106285 creator A5004769237 @default.
• W2137106285 creator A5005804630 @default.
• W2137106285 creator A5010588386 @default.
• W2137106285 creator A5012999223 @default.
• W2137106285 creator A5019698968 @default.
• W2137106285 creator A5022557262 @default.
• W2137106285 creator A5045038056 @default.
• W2137106285 creator A5052503589 @default.
• W2137106285 creator A5059329594 @default.
• W2137106285 creator A5063245254 @default.
• W2137106285 creator A5076828393 @default.
• W2137106285 creator A5089819822 @default.
• W2137106285 date "2010-05-01" @default.
• W2137106285 modified "2023-10-17" @default.
• W2137106285 title "Suppressors of Cytokine Signaling Abrogate Diabetic Nephropathy" @default.
• W2137106285 cites W1538895700 @default.
• W2137106285 cites W1574487823 @default.
• W2137106285 cites W1747473629 @default.
• W2137106285 cites W1946263079 @default.
• W2137106285 cites W1965284496 @default.
• W2137106285 cites W1968531519 @default.
• W2137106285 cites W1973071106 @default.
• W2137106285 cites W1976475029 @default.
• W2137106285 cites W1976915500 @default.
• W2137106285 cites W1977043901 @default.
• W2137106285 cites W2002484874 @default.
• W2137106285 cites W2003582228 @default.
• W2137106285 cites W2004414961 @default.
• W2137106285 cites W2014862688 @default.
• W2137106285 cites W2019667607 @default.
• W2137106285 cites W2021188790 @default.
• W2137106285 cites W2038249890 @default.
• W2137106285 cites W2043867801 @default.
• W2137106285 cites W2046021057 @default.
• W2137106285 cites W2067489934 @default.
• W2137106285 cites W2068604817 @default.
• W2137106285 cites W2072717395 @default.
• W2137106285 cites W2080207036 @default.
• W2137106285 cites W2085133650 @default.
• W2137106285 cites W2093442991 @default.
• W2137106285 cites W2096840133 @default.
• W2137106285 cites W2098208574 @default.
• W2137106285 cites W2098223746 @default.
• W2137106285 cites W2099816894 @default.
• W2137106285 cites W2105487207 @default.
• W2137106285 cites W2105662115 @default.
• W2137106285 cites W2108192985 @default.
• W2137106285 cites W2116415523 @default.
• W2137106285 cites W2117382612 @default.
• W2137106285 cites W2122729097 @default.
• W2137106285 cites W2128219462 @default.
• W2137106285 cites W2132980430 @default.
• W2137106285 cites W2145612190 @default.
• W2137106285 cites W2147363539 @default.
• W2137106285 cites W2150176853 @default.
• W2137106285 cites W2151139199 @default.
• W2137106285 cites W2154523056 @default.
• W2137106285 cites W2155357669 @default.
• W2137106285 cites W2155876350 @default.
• W2137106285 cites W2159864910 @default.
• W2137106285 cites W2170715598 @default.
• W2137106285 doi "https://doi.org/10.1681/asn.2009060625" @default.
• W2137106285 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2865742" @default.
• W2137106285 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20185635" @default.
• W2137106285 hasPublicationYear "2010" @default.
• W2137106285 type Work @default.
• W2137106285 sameAs 2137106285 @default.
• W2137106285 citedByCount "153" @default.
• W2137106285 countsByYear W21371062852012 @default.
• W2137106285 countsByYear W21371062852013 @default.
• W2137106285 countsByYear W21371062852014 @default.
• W2137106285 countsByYear W21371062852015 @default.
• W2137106285 countsByYear W21371062852016 @default.
• W2137106285 countsByYear W21371062852017 @default.
• W2137106285 countsByYear W21371062852018 @default.
• W2137106285 countsByYear W21371062852019 @default.
• W2137106285 countsByYear W21371062852020 @default.
• W2137106285 countsByYear W21371062852021 @default.
• W2137106285 countsByYear W21371062852022 @default.
• W2137106285 countsByYear W21371062852023 @default.
• W2137106285 crossrefType "journal-article" @default.
• W2137106285 hasAuthorship W2137106285A5004769237 @default.
• W2137106285 hasAuthorship W2137106285A5005804630 @default.
• W2137106285 hasAuthorship W2137106285A5010588386 @default.
• W2137106285 hasAuthorship W2137106285A5012999223 @default.
• W2137106285 hasAuthorship W2137106285A5019698968 @default.
• W2137106285 hasAuthorship W2137106285A5022557262 @default.
• W2137106285 hasAuthorship W2137106285A5045038056 @default.
• W2137106285 hasAuthorship W2137106285A5052503589 @default.
• W2137106285 hasAuthorship W2137106285A5059329594 @default.
• W2137106285 hasAuthorship W2137106285A5063245254 @default.
• W2137106285 hasAuthorship W2137106285A5076828393 @default.
• W2137106285 hasAuthorship W2137106285A5089819822 @default.
• W2137106285 hasBestOaLocation W21371062851 @default.
• W2137106285 hasConcept C112392421 @default.
• W2137106285 hasConcept C121608353 @default.

• next