ArticleAging2024
LncRNA DANCR suppresses acute myocardial infarction in mice via mediating p-RXRA/TRAF2/NIK/IKK/NF-κB signaling pathway.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Proteomic aging clocks in epidemiological studies: advances, applications and prospects.Nature aging · 2026Review
- A precision medicine approach to interpret a GATA4 genetic variant in a paediatric patient with congenital heart disease.Human genomics · 2026Article
- NF-Frontiers in cardiovascular medicine · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThis study aimed to investigate the role of LncRNA differentiation antagonizing non-protein coding RNA (DANCR) in acute myocardial infarction (AMI).
methodsA mouse model of AMI was established, and the cardiac contractile function was detected. Next, cardiomyocytes treated with oxygen-glucose deprivation (OGD) were used for gain- and loss-function experiments
resultsThe expression of DANCR in myocardial tissues of AMI mice were significantly downregulated. Overexpression of DANCR decreased myocardial infarct size and enhanced cardiac contractile function in AMI mice. Moreover, overexpression of DANCR promoted proliferation and inhibited apoptosis in OGD-induced cardiomyocytes. Mechanism studies demonstrated that DANCR interacted with RXRA and promoted glycogen synthase kinase 3beta (GSK3β)-mediated phosphorylation of RXRA, and phosphorylated RXRA interacted with TRAF2 protein to downregulate TRAF2 protein level. Bexarotene (Bex), an activator of RXRA, inhibited TRAF2 protein expression, while RXRA overexpression had no effect on TRAF2 protein expression. Bex treatment or silencing TRAF2 promoted proliferation and inhibited apoptosis in cardiomyocytes. In addition, silencing DANCR inhibited cardiomyocyte proliferation and induced apoptosis by activating the NIK/IKK/NF-κB pathway, while B022, an inhibitor of NIK, counteracted the effects of DANCR silencing on cardiomyocytes.
conclusionsStudies demonstrated that DANCR suppressed AMI in mice by mediating p-RXRA/TRAF2/NIK/IKK/NF-κB pathway.
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