ArticleImmunity, inflammation and disease2023
Down-regulation of OIP5-AS1 inhibits obesity-induced myocardial pyroptosis and miR-22/NLRP3 inflammasome axis.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Hydroxytyrosol attenuates obesity-induced myocardial fibrosis by inhibiting NLRP3/CYLD/NOX4 mediated oxidative stress.NPJ science of food · 2026Article
- LncRNA OIP5-AS1 knockdown is associated with attenuated nonylphenol-induced cardiac fibrosis.Environmental health and preventive medicine · 2026Article
- Aerobic exercise mitigates high-fat diet-induced cardiac dysfunction, pyroptosis, and inflammation by inhibiting STING-NLRP3 signaling pathway.Molecular and cellular biochemistry · 2024Article
- Synergistic Effects of Weight Loss and Catheter Ablation: Can microRNAs Serve as Predictive Biomarkers for the Prevention of Atrial Fibrillation Recurrence?International journal of molecular sciences · 2024Review
- Circ_005077 accelerates myocardial lipotoxicity induced by high-fat diet via CyPA/p47PHOX mediated ferroptosis.Cardiovascular diabetology · 2024Article
- Down-regulation of OIP5-AS1 inhibits obesity-induced myocardial pyroptosis and miR-22/NLRP3 inflammasome axis.Immunity, inflammation and disease · 2023Article
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8 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundObesity can induce myocardial pyroptosis, but the exact mechanism is still unknown. A recent study reported the association of opa-interacting protein 5-antisense transcript 1 (OIP5-AS1), an evolutionarily conserved long noncoding RNA, with pyroptosis. Therefore, this study aimed to investigate the role of OIP5-AS1 in obesity-induced myocardial pyroptosis.
methodsOIP5-AS1 was downregulated in H9c2 cells, followed by treatment with 400 μM palmitic acid (PA). Propidium iodide (PI) staining, lactic dehydrogenase (LDH) release assay, caspase-1 activity assay, IL-1β, and IL-18 activity assay were performed to detect pyroptotic phenotype. The interaction between OIP5-AS1 and microRNAs (miRNAs) was analyzed using RNA pull-down and luciferase assay. The effect of OIP5-AS1 knockdown in high-fat diet (HFD)-induced obesity rat on cardiac function, myocardial hypertrophy, fibrosis, and remodeling was evaluated.
resultsFat deposition was observed in cardiomyocytes 24 h after PA treatment; moreover, PA-treated cardiomyocytes showed significant increase in the rate of pyroptotic cells, release of LDH, protein expressions of NLRP3 and cleaved caspase-1, and the activity of caspase-1, IL-1β, and IL-18 as well as OIP5-AS1 expression. These findings suggested that PA activated pyroptosis and induced OIP5-AS1 expression in cardiomyocytes. Moreover, OIP5-AS1 knockdown inhibited PA-induced pyroptosis. Mechanistically, OIP5-AS1 was found to specifically bind to miR-22 and to regulate NLRP3 inflammasome-mediated pyroptosis via miR-22. Furthermore, OIP5-AS1 knockdown ameliorated HFD-induced cardiac dysfunction, myocardial hypertrophy, fibrosis, remodeling, and pyroptosis.
conclusionOur results revealed that downregulation of OIP5-AS1 can inhibit obesity-induced myocardial pyroptosis via miR-22/NLRP3 inflammasome axis. This finding lays a foundation of gene therapy for heart disease targeting OIP5-AS1.
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