ArticleBMC gastroenterology2025
Regulatory effects of miR-30c knockout on hepatic lipid metabolism and progression of liver fibrosis.
Article in BMC gastroenterology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Functional analysis and identification of miRNAs associated with lipid metabolism from milk-derived exosomes.Journal of animal science and biotechnology · 2026Article
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7 authors.
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Abstract
backgroundLiver fibrosis is a chronic progressive liver disease influenced by environmental and genetic factors. Early stages of liver fibrosis are marked by abnormal fat deposition in the liver. MicroRNA-30c (miR-30c) plays key roles in various pathological processes, including lipid metabolism, metabolic disorders, and cancer. However, the precise role of miR-30c in the progression of liver fibrosis remains unclear. This study aimed to investigate the role of miR-30c in liver fibrosis using miR-30c knockout (KO) mice.
methodsKO mice were compared to wild-type (WT) mice to evaluate growth and development, with a focus on lipid metabolism markers. Liver transcriptomic analysis was performed to explore gene expression alterations due to miR-30c knockout. To induce liver fibrosis, thioacetamide (TAA) was administered to the mice, allowing the assessment of the impact of miR-30c on fibrosis initiation and progression.
resultsThe results showed that miR-30c knockout led to body weight loss and disrupted lipid metabolism in mice. A total of 212 upregulated genes and 267 downregulated genes were identified in the livers of KO mice by RNA-seq. Differential enrichment of lipid metabolism pathways was observed KO mice, including PPAR signaling pathway, fatty acid degradation, biosynthesis of unsaturated fatty acids, and so on. The deletion of miR-30c aggravated the liver injury induced by TAA and increased the structural disorder of hepatocytes, and miR-30c knockout mice showed more severe liver fibrosis. This study establishes miR-30c as protective against liver fibrosis progression.
conclusionThe deficiency of miR-30c might exacerbate fibrosis and inflammation, while also disrupting lipid metabolism, suggesting that miR-30c modulation shows therapeutic potential based on mechanistic evidence. Further exploration of miR-30c-mediated crosstalk between metabolic and inflammatory pathways could advance therapeutic strategies for fibrotic liver diseases.
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