FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W3043095167> ?p ?o ?g. }

• W3043095167 endingPage "1995" @default.
• W3043095167 startingPage "1987" @default.
• W3043095167 abstract "Significance Statement Fecal oxalate excretion is critical in oxalate balance with progression of CKD. However, the identity of the transporter(s) responsible for increased intestinal oxalate secretion in CKD is unknown. Intestinal expression of oxalate transporter Slc26a6 is strongly upregulated in two murine models of CKD. Deletion of Slc26a6 completely abrogates enhanced fecal oxalate excretion in CKD, increasing plasma oxalate concentration. This study demonstrates that Slc26a6 mediates intestinal oxalate secretion and mitigates hyperoxalemia in murine CKD models. The findings suggest that pharmacologic approaches enhancing intestinal Slc26a6 activity may stimulate extrarenal clearance of oxalate and prevent hyperoxalemia in CKD. Future studies are needed to address whether similar mechanisms contribute to intestinal oxalate elimination in humans to enhance extrarenal oxalate clearance. Background A state of oxalate homeostasis is maintained in patients with healthy kidney function. However, as GFR declines, plasma oxalate (P ox ) concentrations start to rise. Several groups of researchers have described augmentation of oxalate secretion in the colon in models of CKD, but the oxalate transporters remain unidentified. The oxalate transporter Slc26a6 is a candidate for contributing to the extrarenal clearance of oxalate via the gut in CKD. Methods Feeding a diet high in soluble oxalate or weekly injections of aristolochic acid induced CKD in age- and sex-matched wild-type and Slc26a6 −/− mice. qPCR, immunohistochemistry, and western blot analysis assessed intestinal Slc26a6 expression. An oxalate oxidase assay measured fecal and P ox concentrations. Results Fecal oxalate excretion was enhanced in wild-type mice with CKD. This increase was abrogated in Slc26a6 −/− mice associated with a significant elevation in plasma oxalate concentration. Slc26a6 mRNA and protein expression were greatly increased in the intestine of mice with CKD. Raising P ox without inducing kidney injury did not alter intestinal Slc26a6 expression, suggesting that changes associated with CKD regulate transporter expression rather than elevations in P ox . Conclusions Slc26a6-mediated enteric oxalate secretion is critical in decreasing the body burden of oxalate in murine CKD models. Future studies are needed to address whether similar mechanisms contribute to intestinal oxalate elimination in humans to enhance extrarenal oxalate clearance." @default.
• W3043095167 created "2020-07-23" @default.
• W3043095167 creator A5001244964 @default.
• W3043095167 creator A5014129737 @default.
• W3043095167 creator A5049016107 @default.
• W3043095167 creator A5066682031 @default.
• W3043095167 creator A5066841350 @default.
• W3043095167 creator A5086077605 @default.
• W3043095167 date "2020-07-13" @default.
• W3043095167 modified "2023-10-12" @default.
• W3043095167 title "Enteric Oxalate Secretion Mediated by Slc26a6 Defends against Hyperoxalemia in Murine Models of Chronic Kidney Disease" @default.
• W3043095167 cites W1555045286 @default.
• W3043095167 cites W1896814935 @default.
• W3043095167 cites W1982504166 @default.
• W3043095167 cites W1989402638 @default.
• W3043095167 cites W2001258594 @default.
• W3043095167 cites W2016544862 @default.
• W3043095167 cites W2020675784 @default.
• W3043095167 cites W2037847893 @default.
• W3043095167 cites W2042259238 @default.
• W3043095167 cites W2047638725 @default.
• W3043095167 cites W2057126612 @default.
• W3043095167 cites W2093800807 @default.
• W3043095167 cites W2113263764 @default.
• W3043095167 cites W2129218640 @default.
• W3043095167 cites W2131213184 @default.
• W3043095167 cites W2135799781 @default.
• W3043095167 cites W2142435446 @default.
• W3043095167 cites W2144998523 @default.
• W3043095167 cites W2146048475 @default.
• W3043095167 cites W2146388769 @default.
• W3043095167 cites W2149288036 @default.
• W3043095167 cites W2161566455 @default.
• W3043095167 cites W2168288152 @default.
• W3043095167 cites W2308664293 @default.
• W3043095167 cites W2422348799 @default.
• W3043095167 cites W2889195042 @default.
• W3043095167 cites W2899120878 @default.
• W3043095167 doi "https://doi.org/10.1681/asn.2020010105" @default.
• W3043095167 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7461683" @default.
• W3043095167 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32660969" @default.
• W3043095167 hasPublicationYear "2020" @default.
• W3043095167 type Work @default.
• W3043095167 sameAs 3043095167 @default.
• W3043095167 citedByCount "12" @default.
• W3043095167 countsByYear W30430951672020 @default.
• W3043095167 countsByYear W30430951672021 @default.
• W3043095167 countsByYear W30430951672022 @default.
• W3043095167 countsByYear W30430951672023 @default.
• W3043095167 crossrefType "journal-article" @default.
• W3043095167 hasAuthorship W3043095167A5001244964 @default.
• W3043095167 hasAuthorship W3043095167A5014129737 @default.
• W3043095167 hasAuthorship W3043095167A5049016107 @default.
• W3043095167 hasAuthorship W3043095167A5066682031 @default.
• W3043095167 hasAuthorship W3043095167A5066841350 @default.
• W3043095167 hasAuthorship W3043095167A5086077605 @default.
• W3043095167 hasBestOaLocation W30430951671 @default.
• W3043095167 hasConcept C126322002 @default.
• W3043095167 hasConcept C134018914 @default.
• W3043095167 hasConcept C178790620 @default.
• W3043095167 hasConcept C185592680 @default.
• W3043095167 hasConcept C2776351790 @default.
• W3043095167 hasConcept C2778653478 @default.
• W3043095167 hasConcept C2779403450 @default.
• W3043095167 hasConcept C2780091579 @default.
• W3043095167 hasConcept C71924100 @default.
• W3043095167 hasConceptScore W3043095167C126322002 @default.
• W3043095167 hasConceptScore W3043095167C134018914 @default.
• W3043095167 hasConceptScore W3043095167C178790620 @default.
• W3043095167 hasConceptScore W3043095167C185592680 @default.
• W3043095167 hasConceptScore W3043095167C2776351790 @default.
• W3043095167 hasConceptScore W3043095167C2778653478 @default.
• W3043095167 hasConceptScore W3043095167C2779403450 @default.
• W3043095167 hasConceptScore W3043095167C2780091579 @default.
• W3043095167 hasConceptScore W3043095167C71924100 @default.
• W3043095167 hasFunder F4320311372 @default.
• W3043095167 hasFunder F4320320875 @default.
• W3043095167 hasFunder F4320320879 @default.
• W3043095167 hasFunder F4320332161 @default.
• W3043095167 hasIssue "9" @default.
• W3043095167 hasLocation W30430951671 @default.
• W3043095167 hasLocation W30430951672 @default.
• W3043095167 hasOpenAccess W3043095167 @default.
• W3043095167 hasPrimaryLocation W30430951671 @default.
• W3043095167 hasRelatedWork W196887818 @default.
• W3043095167 hasRelatedWork W2075589613 @default.
• W3043095167 hasRelatedWork W2096390168 @default.
• W3043095167 hasRelatedWork W2748952813 @default.
• W3043095167 hasRelatedWork W2905193867 @default.
• W3043095167 hasRelatedWork W2909197968 @default.
• W3043095167 hasRelatedWork W2993540646 @default.
• W3043095167 hasRelatedWork W3115240940 @default.
• W3043095167 hasRelatedWork W38053709 @default.
• W3043095167 hasRelatedWork W4385893756 @default.
• W3043095167 hasVolume "31" @default.
• W3043095167 isParatext "false" @default.
• W3043095167 isRetracted "false" @default.
• W3043095167 magId "3043095167" @default.

• next