ArticleJournal of cellular and molecular medicine2019
miR-193a/b-3p relieves hepatic fibrosis and restrains proliferation and activation of hepatic stellate cells.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Hsa_circ_0002103 promotes progression of colorectal cancer via miR-193a-3p/CCND1 axis.Molecular and cellular biochemistry · 2026Article
- Article
- GMP-compliant, serum-free cultures preserve therapeutic potential of extracellular vesicles from human mesenchymal stromal cells.Frontiers in cell and developmental biology · 2025Article
- Noncoding RNA-Mediated Epigenetic Regulation in Hepatic Stellate Cells of Liver Fibrosis.Non-coding RNA · 2024Review
- Interplays of liver fibrosis-associated microRNAs: Molecular mechanisms and implications in diagnosis and therapy.Genes & diseases · 2023Review
- MicroRNA Profiling in the Aqueous Humor of Keratoconus Eyes.Translational vision science & technology · 2022Article
- Long Non-Coding RNAInternational journal of molecular sciences · 2022Article
- MicroRNA-193b impairs muscle growth in mouse models of type 2 diabetes by targeting the PDK1/Akt signalling pathway.Diabetologia · 2022Article
- Over-expression of miR-193a-3p regulates the apoptosis of colorectal cancer cells by targeting PAK3.American journal of translational research · 2022Article
- Mig-6 Inhibits Autophagy in HCC Cell Lines by Modulating miR-193a-3p.International journal of medical sciences · 2022Article
- [Regulatory effects of microRNAs on hepatic stellate cell activation and liver fibrogenesis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2021Article
- Mitochondrial transplantation therapy inhibit carbon tetrachloride-induced liver injury through scavenging free radicals and protecting hepatocytes.Bioengineering & translational medicine · 2021Article
- Inhibition of miR-188-5p alleviates hepatic fibrosis by significantly reducing the activation and proliferation of HSCs through PTEN/PI3K/AKT pathway.Journal of cellular and molecular medicine · 2021Article
- Circulatory microRNAs as potential biomarkers for fatty liver disease: the Rotterdam study.Alimentary pharmacology & therapeutics · 2021Article
- MicroRNAs in Transforming Growth Factor-Beta Signaling Pathway Associated With Fibrosis Involving Different Systems of the Human Body.Frontiers in molecular biosciences · 2021Review
- Integrated Analysis of Hepatic miRNA and mRNA Expression Profiles in the Spontaneous Reversal Process of Liver Fibrosis.Frontiers in genetics · 2021Article
- MiR-34c promotes hepatic stellate cell activation and Liver Fibrogenesis by suppressing ACSL1 expression.International journal of medical sciences · 2021Article
- Circular RNAs associated with a mouse model of concanavalin A-induced autoimmune hepatitis: preliminary screening and comprehensive functional analysis.FEBS open bio · 2020Article
- Exosomal miR-223 derived from natural killer cells inhibits hepatic stellate cell activation by suppressing autophagy.Molecular medicine (Cambridge, Mass.) · 2020Article
- Characterization and functional prediction of the microRNAs differentially expressed in a mouse model of concanavalin A-induced autoimmune hepatitis.International journal of medical sciences · 2020Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) have been confirmed to participate in liver fibrosis progression and activation of hepatic stellate cells (HSCs). In this study, the role of miR-193a/b-3p in concanavalin A (ConA)-induced liver fibrosis in mice was evaluated. According to the results, the expression of miR-193a/b-3p was down-regulated in liver tissues after exposure to ConA. Lentivirus-mediated overexpression of miR-193a/b-3p reduced ConA-induced liver injury as demonstrated by decreasing ALT and AST levels. Moreover, ConA-induced liver fibrosis was restrained by the up-regulation of miR-193a/b-3 through inhibiting collagen deposition, decreasing desmin and proliferating cell nuclear antigen (PCNA) expression and lessening the content of hydroxyproline, transforming growth factor-β1 (TGF-β1) and activin A in liver tissues. Furthermore, miR-193a/b-3p mimics suppressed the proliferation of human HSCs LX-2 via inducing the apoptosis of LX-2 cells and lowering the levels of cell cycle-related proteins Cyclin D1, Cyclin E1, p-Rb and CAPRIN1. Finally, TGF-β1 and activin A-mediated activation of LX-2 cells was reversed by miR-193a/b-3p mimics via repressing COL1A1 and α-SMA expression, and restraining the activation of TGF-β/Smad2/3 signalling pathway. CAPRIN1 and TGF-β2 were demonstrated to be the direct target genes of miR-193a/b-3p. We conclude that miR-193a/b-3p overexpression attenuates liver fibrosis through suppressing the proliferation and activation of HSCs. Our data suggest that miR-193a-3p and miR-193b-3p may be new therapeutic targets for liver fibrosis.
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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.