FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2966455586> ?p ?o ?g. }

• W2966455586 abstract "Dicarbonyl stress plays an important role in the pathogenesis of microvascular complications that precede the formation of advanced glycation end products, and contributes to the development of renal dysfunction. In renal cells, toxic metabolites like methylglyoxal lead to mitochondrial dysfunction and protein structure modifications. In our study, we investigated the effect of methylglyoxal on metabolic, transcriptomic, metabolomic and proteomic profiles in the context of the development of kidney impairment in the model of metabolic syndrome. Dicarbonyl stress was induced by intragastric administration of methylglyoxal (0.5 mg/kg bw for 4 weeks) in a strain of hereditary hypertriglyceridaemic rats with insulin resistance and fatty liver. Methylglyoxal administration aggravated glucose intolerance (AUC0–120 p < 0.05), and increased plasma glucose (p < 0.01) and insulin (p < 0.05). Compared to controls, methylglyoxal-treated rats exhibited microalbuminuria (p < 0.01). Targeted proteomic analysis revealed increases in urinary secretion of pro-inflammatory parameters (MCP-1, IL-6, IL-8), specific collagen IV fragments and extracellular matrix proteins. Urine metabolomic biomarkers in methylglyoxal-treated rats were mainly associated with impairment of membrane phospholipids (8-isoprostane, 4-hydroxynonenal). Decreased levels of glutathione (p < 0.01) together with diminished activity of glutathione-dependent antioxidant enzymes contributed to oxidative and dicarbonyl stress. Methylglyoxal administration elevated glyoxalase 1 expression (p < 0.05), involved in methylglyoxal degradation. Based on comparative transcriptomic analysis of the kidney cortex, 96 genes were identified as differentially expressed (FDR < 0.05). Network analysis revealed an over-representation of genes related to oxidative stress and pro-inflammatory signalling pathways as well as an inhibition of angiogenesis suggesting its contribution to renal fibrosis. Our results support the hypothesis that dicarbonyl stress plays a key role in renal microvascular complications. At the transcriptome level, methylglyoxal activated oxidative and pro-inflammatory pathways and inhibited angiogenesis. These effects were further supported by the results of urinary proteomic and metabolomic analyses." @default.
• W2966455586 created "2019-08-13" @default.
• W2966455586 creator A5020872495 @default.
• W2966455586 creator A5023584418 @default.
• W2966455586 creator A5028626429 @default.
• W2966455586 creator A5040702446 @default.
• W2966455586 creator A5042837368 @default.
• W2966455586 creator A5053536763 @default.
• W2966455586 creator A5066798612 @default.
• W2966455586 creator A5083791988 @default.
• W2966455586 date "2019-08-01" @default.
• W2966455586 modified "2023-10-06" @default.
• W2966455586 title "The effect of dicarbonyl stress on the development of kidney dysfunction in metabolic syndrome – a transcriptomic and proteomic approach" @default.
• W2966455586 cites W1190581294 @default.
• W2966455586 cites W1525845993 @default.
• W2966455586 cites W1963648288 @default.
• W2966455586 cites W2009987755 @default.
• W2966455586 cites W2018909053 @default.
• W2966455586 cites W2064820734 @default.
• W2966455586 cites W2081823465 @default.
• W2966455586 cites W2103645063 @default.
• W2966455586 cites W2108192985 @default.
• W2966455586 cites W2110412761 @default.
• W2966455586 cites W2124742398 @default.
• W2966455586 cites W2128160632 @default.
• W2966455586 cites W2133022777 @default.
• W2966455586 cites W2152366277 @default.
• W2966455586 cites W2162143298 @default.
• W2966455586 cites W2167061914 @default.
• W2966455586 cites W2172099178 @default.
• W2966455586 cites W2229996456 @default.
• W2966455586 cites W2258832448 @default.
• W2966455586 cites W2259516816 @default.
• W2966455586 cites W2289876298 @default.
• W2966455586 cites W2293894308 @default.
• W2966455586 cites W2464519895 @default.
• W2966455586 cites W2509824523 @default.
• W2966455586 cites W2511929416 @default.
• W2966455586 cites W2512253971 @default.
• W2966455586 cites W2520929822 @default.
• W2966455586 cites W2529130100 @default.
• W2966455586 cites W2574128142 @default.
• W2966455586 cites W2585465088 @default.
• W2966455586 cites W2605945159 @default.
• W2966455586 cites W2606658423 @default.
• W2966455586 cites W2752001800 @default.
• W2966455586 cites W2890938493 @default.
• W2966455586 cites W2946240089 @default.
• W2966455586 doi "https://doi.org/10.1186/s12986-019-0376-1" @default.
• W2966455586 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6670216" @default.
• W2966455586 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31388341" @default.
• W2966455586 hasPublicationYear "2019" @default.
• W2966455586 type Work @default.
• W2966455586 sameAs 2966455586 @default.
• W2966455586 citedByCount "10" @default.
• W2966455586 countsByYear W29664555862020 @default.
• W2966455586 countsByYear W29664555862021 @default.
• W2966455586 countsByYear W29664555862022 @default.
• W2966455586 countsByYear W29664555862023 @default.
• W2966455586 crossrefType "journal-article" @default.
• W2966455586 hasAuthorship W2966455586A5020872495 @default.
• W2966455586 hasAuthorship W2966455586A5023584418 @default.
• W2966455586 hasAuthorship W2966455586A5028626429 @default.
• W2966455586 hasAuthorship W2966455586A5040702446 @default.
• W2966455586 hasAuthorship W2966455586A5042837368 @default.
• W2966455586 hasAuthorship W2966455586A5053536763 @default.
• W2966455586 hasAuthorship W2966455586A5066798612 @default.
• W2966455586 hasAuthorship W2966455586A5083791988 @default.
• W2966455586 hasBestOaLocation W29664555861 @default.
• W2966455586 hasConcept C104317684 @default.
• W2966455586 hasConcept C126322002 @default.
• W2966455586 hasConcept C129070979 @default.
• W2966455586 hasConcept C134018914 @default.
• W2966455586 hasConcept C147990577 @default.
• W2966455586 hasConcept C150194340 @default.
• W2966455586 hasConcept C162317418 @default.
• W2966455586 hasConcept C181199279 @default.
• W2966455586 hasConcept C185592680 @default.
• W2966455586 hasConcept C2776151105 @default.
• W2966455586 hasConcept C2778592357 @default.
• W2966455586 hasConcept C538909803 @default.
• W2966455586 hasConcept C55493867 @default.
• W2966455586 hasConcept C555293320 @default.
• W2966455586 hasConcept C71924100 @default.
• W2966455586 hasConcept C86803240 @default.
• W2966455586 hasConcept C98274493 @default.
• W2966455586 hasConceptScore W2966455586C104317684 @default.
• W2966455586 hasConceptScore W2966455586C126322002 @default.
• W2966455586 hasConceptScore W2966455586C129070979 @default.
• W2966455586 hasConceptScore W2966455586C134018914 @default.
• W2966455586 hasConceptScore W2966455586C147990577 @default.
• W2966455586 hasConceptScore W2966455586C150194340 @default.
• W2966455586 hasConceptScore W2966455586C162317418 @default.
• W2966455586 hasConceptScore W2966455586C181199279 @default.
• W2966455586 hasConceptScore W2966455586C185592680 @default.
• W2966455586 hasConceptScore W2966455586C2776151105 @default.
• W2966455586 hasConceptScore W2966455586C2778592357 @default.
• W2966455586 hasConceptScore W2966455586C538909803 @default.
• W2966455586 hasConceptScore W2966455586C55493867 @default.
• W2966455586 hasConceptScore W2966455586C555293320 @default.

• next