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LncRNA FAF attenuates hypoxia/ischaemia-induced pyroptosis via the miR-185-5p/PAK2 axis in cardiomyocytes. | LitMetric

AI Article Synopsis

  • Pyroptosis, a form of cell death, is linked to cardiovascular diseases, but the role of long noncoding RNAs (lncRNAs) in regulating this process in heart cells is not well understood.
  • This study investigates the lncRNA FGF9-associated factor (FAF) and its effects on reducing cell death in acute myocardial infarction (AMI) by examining its interaction with miR-185-5p and PAK2 in heart cells exposed to low oxygen.
  • Findings indicate that higher levels of lncRNA FAF can decrease pyroptosis in heart cells, improve cell survival, and lessen damage during AMI, suggesting that the FAF/miR-185-5p/PAK2

Article Abstract

Pyroptosis is associated with various cardiovascular diseases. Increasing evidence suggests that long noncoding RNAs (lncRNAs) have been implicated in gene regulation, but how lncRNAs participate in the regulation of pyroptosis in the heart remains largely unknown. In this study, we aimed to explore the antipyroptotic effects of lncRNA FGF9-associated factor (FAF) in acute myocardial infarction (AMI). The expression patterns of lncRNA FAF, miR-185-5p and P21 activated kinase 2 (PAK2) were detected in hypoxia/ischaemia-induced cardiomyocytes. Hoechst 33342/PI staining, lactate dehydrogenase (LDH) release assay, immunofluorescence and Western blotting were conducted to assay cell pyroptosis. The interaction between lncRNA FAF, miR-185-5p and PAK2 was verified by bioinformatics analysis, small RNA sequencing luciferase reporter assay and qRT-PCR. The expression of LncRNA FAF was downregulated in hypoxic cardiomyocytes and myocardial tissues. Overexpression of lncRNA FAF could attenuate cardiomyocyte pyroptosis, improve cell viability and reduce infarct size during the procession of AMI. Moreover, lncRNA FAF was confirmed as a sponge of miR-185-5p and promoted PAK2 expression in cardiomyocytes. Collectively, our findings reveal a novel lncRNA FAF/miR-185-5p/PAK2 axis as a crucial regulator in cardiomyocyte pyroptosis, which might be a potential therapeutic target of AMI.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9097851PMC
http://dx.doi.org/10.1111/jcmm.17304DOI Listing

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