ArticleCell death discovery2025
Overexpression miR-125a-5p inhibits HSCs activation and alleviates liver fibrosis through TGF-β/Smad2/3 signaling pathway and autophagy.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Therapeutic Targets for Hepatic Fibrosis Driven by Hypoxia-Mediated Hepatic Stellate Cell Activation.Biomolecules · 2026Review
- Hexokinase-3 upregulation and histone H3K18 lactylation mediate murine liver fibrosis induced by Echinococcus multilocularis.PLoS neglected tropical diseases · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis represents an important pathological stage during chronic hepatopathy development, posing a significant threat to human health. Hepatic stellate cells (HSCs), an essential hepatic non-parenchymal cells, have a key effect on fibrogenesis, with their activation being a hallmark of liver fibrosis. MicroRNAs (miRNAs), the small non-coding RNAs, become the critical biomarkers and regulatory molecules in fibrotic processes. Among them, miR-125a-5p is implicated in cancer and inflammatory pathways, yet its functional role and mechanistic involvement in HSC activation remain poorly understood. According to our findings, miR-125a-5p expression was significantly decreased in TGF-β-activated HSC-T6 cells. Notably, ectopic miR-125a-5p overexpression effectively inhibited TGF-β-mediated HSC-T6 activation. Further mechanistic investigations revealed that miR-125a-5p attenuated HSC activation while ameliorating liver fibrosis through regulating the TGF-β/Smad2/3 pathway and autophagy. Additionally, TGFβR1 was miR-125a-5p's target gene. Collectively, miR-125a-5p negatively regulates HSC activation in liver fibrosis, exerting its anti-fibrotic activities through suppressing the TGF-β/Smad2/3 pathway and autophagy modulation.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.