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

**Authors:** Feiyue Xie, Qiuping Ren, Jun He, Menghang Wu

PMC · DOI: 10.1186/s41065-025-00610-5 · Hereditas · 2025-11-29

## TL;DR

This study shows that low levels of miR-223-3p are linked to worse outcomes in hepatitis B-related liver failure and that miR-223-3p protects liver cells by regulating HSP90B1.

## Contribution

The study identifies miR-223-3p as a novel prognostic biomarker and functional regulator of hepatocyte injury in HBV-ACLF via HSP90B1.

## Key findings

- Low miR-223-3p expression correlates with higher disease severity and poor prognosis in HBV-ACLF patients.
- miR-223-3p promotes hepatocyte survival by suppressing apoptosis and modulating HSP90B1.
- miR-223-3p and MELD score are independent predictors of short-term survival in HBV-ACLF.

## Abstract

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.

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.

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.

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.

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.

The online version contains supplementary material available at 10.1186/s41065-025-00610-5.

## Linked entities

- **Genes:** HSP90B1 (heat shock protein 90 beta family member 1) [NCBI Gene 7184]
- **Chemicals:** H2O2 (PubChem CID 784)

## Full-text entities

- **Genes:** HSP90B1 (heat shock protein 90 beta family member 1) [NCBI Gene 7184] {aka ECGP, GP96, GRP94, HEL-S-125m, HEL35, TRA1}
- **Diseases:** acute-on-chronic liver failure (MESH:D065290), hepatocyte injury (MESH:D014947)
- **Species:** Hepatitis B virus (no rank) [taxon 10407]

## Full text

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## Figures

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## References

4 references — full list in the complete paper: https://tomesphere.com/paper/PMC12771722/full.md

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Source: https://tomesphere.com/paper/PMC12771722