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Background <p>Hepatitis 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.</p> Objective <p>The aim was to assess the predictive value of <i>miR-223-3p</i> in the short-term prognosis of patients and its potential role in HBV-ACLF, thus providing new ideas for personalized treatment.</p> Materials and methods <p>The level of <i>miR-223-3p</i> was quantified using qRT-PCR. The correlation between <i>miR-223-3p</i> 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 <i>miR-223-3p</i> 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 <i>miR-223-3p</i>. The regulation between <i>miR-223-3p</i> and <i>HSP90B1</i> was validated through Dual-luciferase reporter gene assay.</p> Results <p>In patients with HBV-ACLF, <i>miR-223-3p</i> expression was reduced and negatively correlated with TBil, INR, and MELD score. Low expression of <i>miR-223-3p</i> predicted adverse prognosis for patients. Furthermore, MELD score and <i>miR-223-3p</i> were identified as independent prognostic factors in patients with HBV-ACLF. In H<sub>2</sub>O<sub>2</sub> or TNF-α–induced MIHA cells, <i>miR-223-3p</i> facilitated cellular proliferation and suppressed apoptosis. The role of <i>miR-223-3p</i> in hepatocyte injury was mediated by <i>HSP90B1</i>.</p> Conclusions <p>Serum <i>miR-223-3p</i> expression was predictive for short-term survival in patients with HBV-ACLF, and <i>miR-223-3p</i> attenuated hepatocellular injury in vitro by modulating <i>HSP90B1</i>.</p>

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miR-223-3p predicts prognosis of hepatitis B virus-related acute-on-chronic liver failure and is involved in hepatocyte injury via HSP90B1

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月29日

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  • Feiyue Xie,
  • Qiuping Ren,
  • Jun He,
  • Menghang Wu

摘要

Background

Hepatitis 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.

Objective

The 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 methods

The 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.

Results

In 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.

Conclusions

Serum 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.