ArticleHereditas2025
miR-223-3p predicts prognosis of hepatitis B virus-related acute-on-chronic liver failure and is involved in hepatocyte injury via HSP90B1.
Article in Hereditas, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Funding
Abstract
backgroundHepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) is a clinical syndrome that presents with acute hepatic decompensation and liver failure in a relatively short time, with a high mortality rate.
objectiveThe aim was to assess the predictive value of miR-223-3p in the short-term prognosis of patients and its potential role in HBV-ACLF, thus providing new ideas for personalized treatment. MATERIALS AND
methodsThe level of miR-223-3p was quantified using qRT-PCR. The correlation between miR-223-3p level and indicators associated with the severity of HBV-ACLF (TBil, INR, and MELD score) was assessed using Spearman’s method. The prognostic value of miR-223-3p in HBV-ACLF was assessed using the ROC curve, Cox regression analysis, and Kaplan-Meier curve. To detect the proliferation and apoptosis of MIHA cells, CCK-8 assay and flow cytometry were employed. Bioinformatics methods were conducted to identify the downstream targets of miR-223-3p. The regulation between miR-223-3p and HSP90B1 was validated through Dual-luciferase reporter gene assay.
resultsIn patients with HBV-ACLF, miR-223-3p expression was reduced and negatively correlated with TBil, INR, and MELD score. Low expression of miR-223-3p predicted adverse prognosis for patients. Furthermore, MELD score and miR-223-3p were identified as independent prognostic factors in patients with HBV-ACLF. In H2O2 or TNF-α–induced MIHA cells, miR-223-3p facilitated cellular proliferation and suppressed apoptosis. The role of miR-223-3p in hepatocyte injury was mediated by HSP90B1.
conclusionsSerum miR-223-3p expression was predictive for short-term survival in patients with HBV-ACLF, and miR-223-3p attenuated hepatocellular injury in vitro by modulating HSP90B1.
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