FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2943831857> ?p ?o ?g. }

• W2943831857 endingPage "665" @default.
• W2943831857 startingPage "655" @default.
• W2943831857 abstract "Downregulation of MALAT1 alleviates saturated fatty acid-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-kappaB axis Pengyu Jia,1 Nan Wu,2 Dalin Jia,1 Yingxian Sun11Department of Cardiology, the First Affiliated Hospital of China Medical University, Shenyang, Liaoning, People‘s Republic of China; 2The Central Laboratory of the First Affiliated Hospital of China Medical University, Shenyang, Liaoning, People‘s Republic of ChinaPurpose: The increased level of saturated fatty acids (SFAs) is found in patients with diabetes, obesity, and other metabolic disorders. SFAs can induce lipotoxic damage to cardiomyocytes, but the mechanism is unclear. The long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) acts as a key regulator in palmitic acid (PA)-induced hepatic steatosis, but its role in PA-induced myocardial lipotoxic injury is still unknown. The aim of this study was to explore the role and underlying mechanism of MALAT1 in PA-induced myocardial lipotoxic injury.Methods: MALAT1 expression in PA-treated human cardiomyocytes (AC16 cells) was detected by RT-qPCR. The effect of MALAT1 on PA-induced myocardial injury was measured by Cell Counting Kit-8, lactate dehydrogenase (LDH), and creatine kinase-MB (CK-MB) assays. Apoptosis was detected by flow cytometry. The activities of cytokines and nuclear factor (NF)-κB were detected by enzyme-linked immunosorbent assay. The interaction between MALAT1 and miR-26a was evaluated by a luciferase reporter assay and RT-qPCR. The regulatory effects of MALAT1 on high mobility group box 1 (HMGB1) expression were evaluated by RT-qPCR and western blotting.Results: MALAT1 was significantly upregulated in cardiomyocytes after PA treatment. Knockdown of MALAT1 increased the viability of PA-treated cardiomyocytes, decreased apoptosis, and reduced the levels of LDH, CK-MB, TNF-α, and IL-1β. Moreover, we found that MALAT1 specifically binds to miR-26a and observed a reciprocal negative regulatory relationship between these factors. We further found that the downregulation of MALAT1 represses HMGB1 expression, thereby inhibiting the activation of the Toll-like receptor 4 (TLR4)/NF-κB-mediated inflammatory response. These repressive effects were rescued by an miR-26a inhibitor.Conclusion: We demonstrate that MALAT1 is induced by SFAs and its downregulation alleviates SFA-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-κB axis. Our findings provide new insight into the mechanism underlying myocardial lipotoxic injury.Keywords: metastasis-associated lung adenocarcinoma transcript 1, saturated fatty acids, microRNA, high mobility group box-1 protein, inflammation" @default.
• W2943831857 created "2019-05-09" @default.
• W2943831857 creator A5003561300 @default.
• W2943831857 creator A5004402528 @default.
• W2943831857 creator A5073165165 @default.
• W2943831857 creator A5083049118 @default.
• W2943831857 date "2019-05-01" @default.
• W2943831857 modified "2023-10-18" @default.
• W2943831857 title "<p>Downregulation of MALAT1 alleviates saturated fatty acid-induced myocardial inflammatory injury via the miR-26a/HMGB1/TLR4/NF-κB axis</p>" @default.
• W2943831857 cites W1023167256 @default.
• W2943831857 cites W1082427047 @default.
• W2943831857 cites W1982481096 @default.
• W2943831857 cites W2008468705 @default.
• W2943831857 cites W2019055887 @default.
• W2943831857 cites W2035536340 @default.
• W2943831857 cites W2041492579 @default.
• W2943831857 cites W2043442527 @default.
• W2943831857 cites W2058970225 @default.
• W2943831857 cites W2098437467 @default.
• W2943831857 cites W2128619556 @default.
• W2943831857 cites W2163802438 @default.
• W2943831857 cites W2170597525 @default.
• W2943831857 cites W2223740898 @default.
• W2943831857 cites W2284080609 @default.
• W2943831857 cites W2292599350 @default.
• W2943831857 cites W2480155835 @default.
• W2943831857 cites W2511229996 @default.
• W2943831857 cites W2551521661 @default.
• W2943831857 cites W2564043905 @default.
• W2943831857 cites W2572870642 @default.
• W2943831857 cites W2587151574 @default.
• W2943831857 cites W2741985169 @default.
• W2943831857 cites W2747587520 @default.
• W2943831857 cites W2750880769 @default.
• W2943831857 cites W2752183093 @default.
• W2943831857 cites W2768119587 @default.
• W2943831857 cites W2775837711 @default.
• W2943831857 cites W2783821648 @default.
• W2943831857 doi "https://doi.org/10.2147/dmso.s203151" @default.
• W2943831857 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6511247" @default.
• W2943831857 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31123414" @default.
• W2943831857 hasPublicationYear "2019" @default.
• W2943831857 type Work @default.
• W2943831857 sameAs 2943831857 @default.
• W2943831857 citedByCount "26" @default.
• W2943831857 countsByYear W29438318572019 @default.
• W2943831857 countsByYear W29438318572020 @default.
• W2943831857 countsByYear W29438318572021 @default.
• W2943831857 countsByYear W29438318572022 @default.
• W2943831857 countsByYear W29438318572023 @default.
• W2943831857 crossrefType "journal-article" @default.
• W2943831857 hasAuthorship W2943831857A5003561300 @default.
• W2943831857 hasAuthorship W2943831857A5004402528 @default.
• W2943831857 hasAuthorship W2943831857A5073165165 @default.
• W2943831857 hasAuthorship W2943831857A5083049118 @default.
• W2943831857 hasBestOaLocation W29438318571 @default.
• W2943831857 hasConcept C104317684 @default.
• W2943831857 hasConcept C126322002 @default.
• W2943831857 hasConcept C127561419 @default.
• W2943831857 hasConcept C134018914 @default.
• W2943831857 hasConcept C153911025 @default.
• W2943831857 hasConcept C173396325 @default.
• W2943831857 hasConcept C185592680 @default.
• W2943831857 hasConcept C190283241 @default.
• W2943831857 hasConcept C2776914184 @default.
• W2943831857 hasConcept C2779134362 @default.
• W2943831857 hasConcept C2780545709 @default.
• W2943831857 hasConcept C502942594 @default.
• W2943831857 hasConcept C53227056 @default.
• W2943831857 hasConcept C55493867 @default.
• W2943831857 hasConcept C62203573 @default.
• W2943831857 hasConcept C71924100 @default.
• W2943831857 hasConcept C86803240 @default.
• W2943831857 hasConceptScore W2943831857C104317684 @default.
• W2943831857 hasConceptScore W2943831857C126322002 @default.
• W2943831857 hasConceptScore W2943831857C127561419 @default.
• W2943831857 hasConceptScore W2943831857C134018914 @default.
• W2943831857 hasConceptScore W2943831857C153911025 @default.
• W2943831857 hasConceptScore W2943831857C173396325 @default.
• W2943831857 hasConceptScore W2943831857C185592680 @default.
• W2943831857 hasConceptScore W2943831857C190283241 @default.
• W2943831857 hasConceptScore W2943831857C2776914184 @default.
• W2943831857 hasConceptScore W2943831857C2779134362 @default.
• W2943831857 hasConceptScore W2943831857C2780545709 @default.
• W2943831857 hasConceptScore W2943831857C502942594 @default.
• W2943831857 hasConceptScore W2943831857C53227056 @default.
• W2943831857 hasConceptScore W2943831857C55493867 @default.
• W2943831857 hasConceptScore W2943831857C62203573 @default.
• W2943831857 hasConceptScore W2943831857C71924100 @default.
• W2943831857 hasConceptScore W2943831857C86803240 @default.
• W2943831857 hasLocation W29438318571 @default.
• W2943831857 hasLocation W29438318572 @default.
• W2943831857 hasLocation W29438318573 @default.
• W2943831857 hasLocation W29438318574 @default.
• W2943831857 hasOpenAccess W2943831857 @default.
• W2943831857 hasPrimaryLocation W29438318571 @default.
• W2943831857 hasRelatedWork W2020449916 @default.
• W2943831857 hasRelatedWork W2025703417 @default.

• next