FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2967402014> ?p ?o ?g. }

• W2967402014 endingPage "1345" @default.
• W2967402014 startingPage "1332" @default.
• W2967402014 abstract "Chronic kidney disease presents a complex and distinct pathological landscape in men and women, yet this difference is poorly understood. microRNAs are powerful molecular regulators of pathophysiology in the kidney and other organs. We previously reported a significant upregulation of miR-146b-5p in the 5/6 nephrectomy rat model of chronic kidney disease. Here we investigated the sex-specific contribution of miR-146b-5p to renocardiac pathology by generating a novel miR-146b-/- rat and characterized the expression of miR-146b-5p in both wild-type and knockout animals. The 5/6 nephrectomy or sham surgery was performed on rats of each genotype and sex. Renal pathology was examined through gross histology, plasma and urinary analysis of electrolytes and metabolites, and by chronic blood pressure monitoring. Cardiac pathology was monitored via echocardiography and pressure-volume analysis. The miR-146b-/- rats show functional knockout of miR-146b-5p in both the kidney and heart. While 5/6 nephrectomy induced tissue hypertrophy, miR-146b-/- female rats displayed exacerbated renal hypertrophy. Additionally, miR-146b-/- female rats exhibited a marked elevation of renal fibrosis and significant renal dysfunction yet lower blood pressure and less pronounced cardiac remodeling. These phenotypic differences were not exhibited in miR-146b-/- male rats. Ovariectomy ameliorated renal pathology and abolished genotypic differences. In vitro examination of transforming growth factor-β signaling in combination with miR-146b-5p manipulation supports a role for miR-146b-5p in mediating the protective benefit of estrogen from renal pathologies. Thus, our data highlight an important role of miR-146b-5p in modulating kidney disease progression and provide new avenues for the study of sex-specific pathology. Chronic kidney disease presents a complex and distinct pathological landscape in men and women, yet this difference is poorly understood. microRNAs are powerful molecular regulators of pathophysiology in the kidney and other organs. We previously reported a significant upregulation of miR-146b-5p in the 5/6 nephrectomy rat model of chronic kidney disease. Here we investigated the sex-specific contribution of miR-146b-5p to renocardiac pathology by generating a novel miR-146b-/- rat and characterized the expression of miR-146b-5p in both wild-type and knockout animals. The 5/6 nephrectomy or sham surgery was performed on rats of each genotype and sex. Renal pathology was examined through gross histology, plasma and urinary analysis of electrolytes and metabolites, and by chronic blood pressure monitoring. Cardiac pathology was monitored via echocardiography and pressure-volume analysis. The miR-146b-/- rats show functional knockout of miR-146b-5p in both the kidney and heart. While 5/6 nephrectomy induced tissue hypertrophy, miR-146b-/- female rats displayed exacerbated renal hypertrophy. Additionally, miR-146b-/- female rats exhibited a marked elevation of renal fibrosis and significant renal dysfunction yet lower blood pressure and less pronounced cardiac remodeling. These phenotypic differences were not exhibited in miR-146b-/- male rats. Ovariectomy ameliorated renal pathology and abolished genotypic differences. In vitro examination of transforming growth factor-β signaling in combination with miR-146b-5p manipulation supports a role for miR-146b-5p in mediating the protective benefit of estrogen from renal pathologies. Thus, our data highlight an important role of miR-146b-5p in modulating kidney disease progression and provide new avenues for the study of sex-specific pathology. In this issueKidney InternationalVol. 96Issue 6PreviewSeveral omics platforms currently are being used for biomarker discovery. Data integration from multiple platforms while simultaneously accounting for clinical variables is only beginning to be attempted. Kammer and colleagues were interested in identifying prognostic biomarkers for rapid progression of chronic kidney disease (CKD) in patients with type 2 diabetes. They used a novel Bayesian approach to analyze clinical, proteomic, metabolomic, and lipidomic data from patients whose CKD progressed rapidly or remained stable. Full-Text PDF Are women more susceptible to renal dysfunction than men?Kidney InternationalVol. 96Issue 6PreviewIs there any difference in sensitivity to kidney function between men and women? Paterson et al. have focused on sex differences in chronic kidney disease. Surprisingly, their experimental results show that only one microRNA, miR-146b-5p, affected the susceptibility of renocardiac pathology. They generated miR-146b knockout rats and found that miR-146b−/− females developed exacerbated renal hypertrophy and fibrosis and had less cardiac remodeling. Although miR-146b-5p has been reported to be upregulated in various types of cancers, this article reveals the novel role of miR-146b in the kidney. Full-Text PDF" @default.
• W2967402014 created "2019-08-22" @default.
• W2967402014 creator A5031428652 @default.
• W2967402014 creator A5037602755 @default.
• W2967402014 creator A5044300856 @default.
• W2967402014 date "2019-12-01" @default.
• W2967402014 modified "2023-10-16" @default.
• W2967402014 title "miR-146b-5p has a sex-specific role in renal and cardiac pathology in a rat model of chronic kidney disease" @default.
• W2967402014 cites W1964082961 @default.
• W2967402014 cites W1984261234 @default.
• W2967402014 cites W1987216226 @default.
• W2967402014 cites W2012816393 @default.
• W2967402014 cites W2057353595 @default.
• W2967402014 cites W2058109674 @default.
• W2967402014 cites W2059357290 @default.
• W2967402014 cites W2065096751 @default.
• W2967402014 cites W2073789348 @default.
• W2967402014 cites W2077462602 @default.
• W2967402014 cites W2093248070 @default.
• W2967402014 cites W2097888088 @default.
• W2967402014 cites W2109214362 @default.
• W2967402014 cites W2119754755 @default.
• W2967402014 cites W2123295328 @default.
• W2967402014 cites W2128747520 @default.
• W2967402014 cites W2132803823 @default.
• W2967402014 cites W2134629862 @default.
• W2967402014 cites W2135480559 @default.
• W2967402014 cites W2138692579 @default.
• W2967402014 cites W2138874874 @default.
• W2967402014 cites W2141002983 @default.
• W2967402014 cites W2145561964 @default.
• W2967402014 cites W2149030597 @default.
• W2967402014 cites W2158691322 @default.
• W2967402014 cites W2164249826 @default.
• W2967402014 cites W2186358774 @default.
• W2967402014 cites W2200226739 @default.
• W2967402014 cites W2587829329 @default.
• W2967402014 cites W2729069035 @default.
• W2967402014 cites W2740145423 @default.
• W2967402014 cites W2741023509 @default.
• W2967402014 cites W2785099367 @default.
• W2967402014 cites W2884706137 @default.
• W2967402014 cites W2910979721 @default.
• W2967402014 cites W4245235758 @default.
• W2967402014 doi "https://doi.org/10.1016/j.kint.2019.07.017" @default.
• W2967402014 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6941490" @default.
• W2967402014 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31668631" @default.
• W2967402014 hasPublicationYear "2019" @default.
• W2967402014 type Work @default.
• W2967402014 sameAs 2967402014 @default.
• W2967402014 citedByCount "25" @default.
• W2967402014 countsByYear W29674020142019 @default.
• W2967402014 countsByYear W29674020142020 @default.
• W2967402014 countsByYear W29674020142021 @default.
• W2967402014 countsByYear W29674020142022 @default.
• W2967402014 countsByYear W29674020142023 @default.
• W2967402014 crossrefType "journal-article" @default.
• W2967402014 hasAuthorship W2967402014A5031428652 @default.
• W2967402014 hasAuthorship W2967402014A5037602755 @default.
• W2967402014 hasAuthorship W2967402014A5044300856 @default.
• W2967402014 hasBestOaLocation W29674020142 @default.
• W2967402014 hasConcept C10162356 @default.
• W2967402014 hasConcept C126322002 @default.
• W2967402014 hasConcept C133397671 @default.
• W2967402014 hasConcept C134018914 @default.
• W2967402014 hasConcept C142724271 @default.
• W2967402014 hasConcept C2778653478 @default.
• W2967402014 hasConcept C2780091579 @default.
• W2967402014 hasConcept C2780227381 @default.
• W2967402014 hasConcept C2780559512 @default.
• W2967402014 hasConcept C71924100 @default.
• W2967402014 hasConceptScore W2967402014C10162356 @default.
• W2967402014 hasConceptScore W2967402014C126322002 @default.
• W2967402014 hasConceptScore W2967402014C133397671 @default.
• W2967402014 hasConceptScore W2967402014C134018914 @default.
• W2967402014 hasConceptScore W2967402014C142724271 @default.
• W2967402014 hasConceptScore W2967402014C2778653478 @default.
• W2967402014 hasConceptScore W2967402014C2780091579 @default.
• W2967402014 hasConceptScore W2967402014C2780227381 @default.
• W2967402014 hasConceptScore W2967402014C2780559512 @default.
• W2967402014 hasConceptScore W2967402014C71924100 @default.
• W2967402014 hasFunder F4320306230 @default.
• W2967402014 hasFunder F4320332161 @default.
• W2967402014 hasIssue "6" @default.
• W2967402014 hasLocation W29674020141 @default.
• W2967402014 hasLocation W29674020142 @default.
• W2967402014 hasLocation W29674020143 @default.
• W2967402014 hasOpenAccess W2967402014 @default.
• W2967402014 hasPrimaryLocation W29674020141 @default.
• W2967402014 hasRelatedWork W1918853894 @default.
• W2967402014 hasRelatedWork W1966400367 @default.
• W2967402014 hasRelatedWork W2072431089 @default.
• W2967402014 hasRelatedWork W2075462345 @default.
• W2967402014 hasRelatedWork W2086431532 @default.
• W2967402014 hasRelatedWork W2091288360 @default.
• W2967402014 hasRelatedWork W2108194042 @default.
• W2967402014 hasRelatedWork W2750396534 @default.
• W2967402014 hasRelatedWork W2795386776 @default.

• next