ArticleMolecular medicine reports2019
MicroRNA‑219 overexpression serves a protective role during liver fibrosis by targeting tumor growth factor β receptor 2.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Molecular insights into hereditary elliptocytosis and pyropoikilocytosis: NGS uncovers multiple potential candidate genes.Annals of hematology · 2023Article
- Interplays of liver fibrosis-associated microRNAs: Molecular mechanisms and implications in diagnosis and therapy.Genes & diseases · 2023Review
- [Study of the negative regulation of transforming growth factor beta type II receptor to inhibit the occurrence and development of liver fibrosis with miR-217].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2022Article
- Green Synthesis of Silymarin-Chitosan Nanoparticles as a New Nano Formulation with Enhanced Anti-Fibrotic Effects against Liver Fibrosis.International journal of molecular sciences · 2022Article
- MicroRNA-15a inhibits hepatic stellate cell activation and proliferation via targeting SRY-box transcription factor 9.Bioengineered · 2022Article
- Article
- The role of let-7b in the inhibition of hepatic stellate cell activation by rSjP40.PLoS neglected tropical diseases · 2021Article
- MicroRNA-219c-5p regulates bladder fibrosis by targeting FN1.BMC urology · 2020Article
- Crosstalk network among multiple inflammatory mediators in liver fibrosis.World journal of gastroenterology · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive liver fibrosis is the primary cause of liver cirrhosis and hepatocellular carcinoma, and leads to considerable morbidity and mortality. Recent studies have demonstrated that microRNAs (miRNAs or miRs) are associated with fibrotic processes in liver disorders, although the exact role of miR‑219 remains unclear and the relevant mechanisms remain to be completely understood. To the best of our knowledge, the present study was the first to demonstrate the functional implications of miR‑219 expression during liver fibrosis. The present study reported that miR‑219 exhibited significantly reduced expression in serum from patients and that its expression was negatively associated with clinical stage. It was also demonstrated that miR‑219 attenuated angiotensin II‑induced expression of pro‑fibrotic markers, including α‑smooth muscle actin, atlastin GTPase 1 and collagen. Additionally, a CCl4‑induced mouse liver injury model was used to demonstrate that miR‑219 strongly suppressed liver fibrosis in vivo. Furthermore, the present study identified tumor growth factor β receptor 2 (TGFBR2) as a direct target gene of miR‑219. In conclusion, the results of the present study revealed that miR‑219 may regulate pro‑fibrotic markers by directly targeting the TGFBR2 gene and the miR‑219/TGFBR2 signaling pathway may be a potential therapeutic target for liver fibrosis.
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