2022
DOI: 10.1177/02676591221076788
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LINC00936 exacerbated myocardial infarction progression via miR-4795-3p/Wnt3a signaling pathway based on biological and imaging methods

Abstract: Objective LncRNAs show great potential in diagnosing and treating myocardial infarction (MI). Clarifying the mechanism of lncRNAs on MI is of great significance for the application of MI biomarkers. Therefore, this report intended to determine the role and mechanism of LINC00936 on MI by biological and imaging methods. Methods Hypoxia H9C2 model was established by hypoxia treatment. Flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assay detected the apoptosis of H9C2. H2DCFDA sta… Show more

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Cited by 2 publications
(2 citation statements)
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“…26 ATP2B1-AS1, a novel lncRNA, is highly expressed in cerebral ischemia/reperfusion injury 16 and myocardial infarction. 13,27 In line with these findings, our results consistently revealed level of TLR4 and its downstream protein p65 (Figure 5D). Moreover, silencing of ATP2B1-AS1 observably reduced the relative TLR4 mRNA level, and LPS induced the relative TLR4 mRNA level in THP-1 cells (Figure 5E).…”
Section: Atp2b1-as1 Could Bind Mir-23a-3psupporting
confidence: 88%
“…26 ATP2B1-AS1, a novel lncRNA, is highly expressed in cerebral ischemia/reperfusion injury 16 and myocardial infarction. 13,27 In line with these findings, our results consistently revealed level of TLR4 and its downstream protein p65 (Figure 5D). Moreover, silencing of ATP2B1-AS1 observably reduced the relative TLR4 mRNA level, and LPS induced the relative TLR4 mRNA level in THP-1 cells (Figure 5E).…”
Section: Atp2b1-as1 Could Bind Mir-23a-3psupporting
confidence: 88%
“… 41 Using a homologous peptide fragment of Wnt3a to block Frizzled signaling decreased infarct expansion and ameliorated heart remodeling. 37 In vitro, Wnt3a has been shown to exacerbate cardiomyocyte apoptosis induced by hypoxia 42 , 43 and increase caspase activity in NRCMs undergoing hypoxia/reoxygenation injury. 44 Furthermore, cardiomyocyte‐specific deletion of β‐catenin improved cardiac function and LV remodeling after MI by promoting cardiac progenitor cell proliferation.…”
Section: Discussionmentioning
confidence: 99%