ArticleJournal of molecular medicine (Berlin, Germany)2022
TGF-β1/Smad3 upregulates UCA1 to promote liver fibrosis through DKK1 and miR18a.
Article in Journal of molecular medicine (Berlin, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Transcriptomic Identification of Diagnostic Biomarkers for Alcohol-Associated Liver Cirrhosis: Integration of Population-Level Epidemiology with Multi-Cohort Transcriptomic Analysis.International journal of molecular sciences · 2026Article
- IL-10 attenuates metabolic dysfunction-associated steatotic liver disease via modulation of hepatic responses to lipotoxicity.JCI insight · 2026Article
- Innovative analysis and future prospects of Bupleuri Radix's pharmacology and toxicity based on the gut-liver axis.MedScience · 2026Review
- [Cajanonic acid A derivative XJ-60 improves liver fibrosis in mice with non-alcoholic fatty liver disease by inhibiting the SP1/TGF-β/Smad3 signaling axis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- COL1A2 and APOLD1 Define a Dual-Axis Molecular Framework for Diabetic Nephropathy-Retinopathy Comorbidity: An Integrative Multiomics and Machine Learning Study in Mouse Models.International journal of medical sciences · 2026Article
- Proteomic analysis of 7-octenoic acid antifibrotic effects in TGF-β1 activated hepatic stellate cells.Scientific reports · 2025Article
- Linc01271 promotes lipid synthesis and MASLD/MASH progression via miR-149-3p/RAB35 axis.Cellular and molecular life sciences : CMLS · 2025Article
- Gut Microbiota as a Mediator Between Intestinal Fibrosis and Creeping Fat in Crohn's Disease.United European gastroenterology journal · 2025Review
- LncRNA PVT1 activated by TGF-β1/Smad3 facilitates proliferation and metastasis of hepatocellular carcinoma via upregulating Smad6 and NRG1.Journal of translational medicine · 2025Article
- Review
- The interactive role of microRNA and other non-coding RNA in hepatitis B (HBV) associated fibrogenesis.Functional & integrative genomics · 2025Review
- Acupotomy Alleviates Capsular Fibrosis in Frozen Shoulder Rats by Modulating CCL2 to Inhibit Macrophage Recruitment and Suppress the Inflammatory Response.Journal of inflammation research · 2025Article
- Implications in Cancer of Nuclear Micro RNAs, Long Non-Coding RNAs, and Circular RNAs Bound by PRC2 and FUS.Cancers · 2024Review
- KIF18A inactivates hepatic stellate cells and alleviates liver fibrosis through the TTC3/Akt/mTOR pathway.Cellular and molecular life sciences : CMLS · 2024Article
- Retinoid X receptor heterodimers in hepatic function: structural insights and therapeutic potential.Frontiers in pharmacology · 2024Review
- SKIL/SnoN attenuates TGF-β1/SMAD signaling-dependent collagen synthesis in hepatic fibrosis.Biomolecules & biomedicine · 2023Article
- Long non-coding RNAs: key regulators of liver and kidney fibrogenesis.BMB reports · 2023Review
- Fibrosis-the tale of H3K27 histone methyltransferases and demethylases.Frontiers in cell and developmental biology · 2023Review
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
TGF-β1 is the strongest cytokine known to promote liver fibrosis. It has been previously demonstrated that the activation of TGF-β1 initiates a temporary collagen accumulation program, which is important for wound repair in several organs. Furthermore, temporary extracellular matrix enhancement often leads to progressive fibrosis, which is accountable for cases of severe morbidity and mortality worldwide. However, its action mechanism has not been fully explored. It was previously reported that UCA1 could promote its occurrence and development in various tumors. Importantly, it was reported that TGF-β1 could activate the expression of UCA1 in liver cancer, gastric cancer, and breast cancer. However, the role of UCA1 in organ fibrosis, including liver fibrosis, remains unreported. The present study reported for the first time that TGF-β1/Smad3 could promote liver fibrosis by upregulating UCA1, which further affected DKK1 and collagen, such as COL1A1, COL1A2, and COL3A1. Meanwhile, UCA1 could competitively bind with miR18a to stabilize Smad3 to constitute a positive feedback pathway, which played a significant role in the promotion of liver fibrosis. Altogether, the present study provides a theoretical basis for devising promising treatment strategies for liver fibrosis. KEY MESSAGES : UCA1 was found to promote the progression of liver fibrosis in vitro. UCA1 is regulated by TGF-β1 and promotes liver fibrosis through the canonical Smad pathway. UCA1 can competitively bind with miR18a, promote liver fibrosis by stabilizing Smad3, and form a UCA1-miR18a/Smad3 positive feedback. UCA1 binds EZH2 to inhibit the DKK1 expression and promote liver fibrosis.
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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 OpenQuestion graph.