ArticleInternational journal of molecular sciences2022
MicroRNA-223 Suppresses Human Hepatic Stellate Cell Activation Partly via Regulating the Actin Cytoskeleton and Alleviates Fibrosis in Organoid Models of Liver Injury.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Clinicopathological role of microRNA-205, microRNA-223 and microRNA-590 in vulvar cancer.Oncology letters · 2026Article
- ZNF469 drives TGF-β1/SMAD3-mediated extracellular matrix regulation in pulmonary fibrosis.Biomolecules & biomedicine · 2026Article
- Fibrotic microRNAs in the suppression of HSC activation and ECM deposition to facilitate the regression of hepatic fibrosis in zebrafish.Journal of molecular medicine (Berlin, Germany) · 2026Article
- MicroRNAs as Key Regulators in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease: A Bioinformatics Analysis.Biomedicines · 2026Article
- Evaluation of miRNA Expression in Pediatric Cirrhosis Caused by BA and PFIC.BioMed research international · 2026Article
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Pathogenesis of metabolic dysfunction-associated steatotic liver disease and donor liver damage.iLIVER · 2025Review
- ZNF469 promotes extracellular matrix production in normal and keloid dermal fibroblasts.Molecular medicine reports · 2025Article
- Review
- Long non-coding RNAJournal of biomedical research · 2025Article
- Neutrophils in MASLD and MASH.BMB reports · 2025Review
- Liver-derived Exosomal miRNA in NAFLD: Mechanisms of Action, Biomarkers, and Therapeutic Applications.Current medicinal chemistry · 2025Review
- MicroRNA-372-3p impairs fatty acid metabolism in hepatocellular carcinoma cells by targetingBioImpacts : BI · 2025Article
- Role of micrornas in the pathophysiology and diagnosis of metabolic dysfunction-associated steatotic liver disease: A bibliometric review.Hepatology forum · 2025Review
- MicroRNA-223-3p levels in serum-derived extracellular vesicles predict regression of M2BPGi-based liver fibrosis after hepatitis C virus eradication by direct-acting antiviral agents.Journal of gastroenterology · 2024Article
- Regulatory Functions and Mechanisms of Circular RNAs in Hepatic Stellate Cell Activation and Liver Fibrosis.Cells · 2023Review
- Long non-coding RNA H19 promotes proliferation in hepatocellular carcinoma cells via H19/miR-107/CDK6 axis.Oncology research · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
MicroRNAs (miRNAs) are small, non-coding RNAs that negatively regulate target mRNA expression, and altered expression of miRNAs is associated with liver pathological conditions. Recent studies in animal models have shown neutrophil/myeloid-specific microRNA-223 (miR-223) as a key regulator in the development of various liver diseases including fibrosis, where hepatic stellate cells (HSCs) are the key player in pathogenesis. However, the precise roles of miR-223 in human HSCs and its therapeutic potential to control fibrosis remain largely unexplored. Using primary human HSCs, we demonstrated that miR-223 suppressed the fibrogenic program and cellular proliferation while promoting features of quiescent HSCs including lipid re-accumulation and retinol storage. Furthermore, induction of miR-223 in HSCs decreased cellular motility and contraction. Mechanistically, miR-223 negatively regulated expression of smooth muscle α-actin (α-SMA) and thus reduced cytoskeletal activity, which is known to promote amplification of fibrogenic signals. Restoration of α-SMA in miR-223-overexpressing HSCs alleviated the antifibrotic effects of miR-223. Finally, to explore the therapeutic potential of miR-233 in liver fibrosis, we generated co-cultured organoids of HSCs with Huh7 hepatoma cells and challenged them with acetaminophen (APAP) or palmitic acid (PA) to induce hepatotoxicity. We showed that ectopic expression of miR-223 in HSCs attenuated fibrogenesis in the two human organoid models of liver injury, suggesting its potential application in antifibrotic therapy.
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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 OpenQuestion graph.