ArticleOncotarget2017
Antagonism of Interleukin-17A ameliorates experimental hepatic fibrosis by restoring the IL-10/STAT3-suppressed autophagy in hepatocytes.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Role of IL-17 cytokines in tubal fibrosis and infertility due to salpingitis.Molecular biology reports · 2025Review
- Assessing brodalumab in the treatment of primary sclerosing cholangitis (SABR-PSC pilot study): protocol for a single-arm, multicentre, pilot study.BMJ open gastroenterology · 2025Article
- The role of the interleukin family in liver fibrosis.Frontiers in immunology · 2025Review
- IL-17 Signaling in Primary Sclerosing Cholangitis Patient-Derived Organoids.Research square · 2023Article
- The research development of STAT3 in hepatic ischemia-reperfusion injury.Frontiers in immunology · 2023Review
- Interleukin-10 regulates starvation-induced autophagy through the STAT3-mTOR-p70s6k axis in hepatic stellate cells.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- The gut-liver axis in immune remodeling of hepatic cirrhosis.Frontiers in immunology · 2022Review
- Comprehensive bioinformatics and machine learning analysis identify VCAN as a novel biomarker of hepatitis B virus-related liver fibrosis.Frontiers in molecular biosciences · 2022Article
- Review
- Relationship between NAFLD and Periodontal Disease from the View of Clinical and Basic Research, and Immunological Response.International journal of molecular sciences · 2021Review
- The interplay of microRNAs and transcription factors in autophagy regulation in nonalcoholic fatty liver disease.Experimental & molecular medicine · 2021Review
- Autophagy in liver diseases.World journal of hepatology · 2021Review
- Retinoic Acid: A New Old Friend of IL-17A in the Immune Pathogeny of Liver Fibrosis.Frontiers in immunology · 2021Review
- Resveratrol contributes to the inhibition of liver fibrosis by inducing autophagy via the microRNA‑20a‑mediated activation of the PTEN/PI3K/AKT signaling pathway.International journal of molecular medicine · 2020Article
- Fibrosis: from mechanisms to medicines.Nature · 2020Review
- The Effect of Matrix Stiffness on Human Hepatocyte Migration and Function-An In Vitro Research.Polymers · 2020Article
- Disrupting the TRIB3-SQSTM1 interaction reduces liver fibrosis by restoring autophagy and suppressing exosome-mediated HSC activation.Autophagy · 2020Article
- Crosstalk network among multiple inflammatory mediators in liver fibrosis.World journal of gastroenterology · 2019Review
- Improvement in affinity and thermostability of a fully human antibody against interleukin-17A by yeast-display technology and CDR grafting.Acta pharmaceutica Sinica. B · 2019Article
- Fibrogenesis in Chronic DSS Colitis is Not Influenced by Neutralisation of Regulatory T Cells, of Major T Helper Cytokines or Absence of IL-13.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-17A has been identified as a driver of hepatic stellate cell activation and plays a critical role in the pathogenesis of hepatic fibrosis. However, the underlining fibrosis-promoting mechanism of IL-17A is far from understood. Here we aimed to define whether hepatocytes directly respond to IL-17A stimulation and are associated with the development of hepatic fibrosis. The functional significance of IL-17A was evaluated in bile duct ligation (BDL) or thioacetamide (TAA) injection-induced mouse models of hepatic fibrosis. Human cirrhosis and control tissues were obtained from the patients with cirrhosis who received an open surgical repair process. Neutralizing IL-17A promoted the resolution of BDL or TAA-induced acute or chronic inflammation and fibrosis, resulted in a shift of the suppressive immune response in fibrotic liver toward a Th1-type immune response, and restored autophagy activity in both cholestatic and hepatotoxic liver injury induced fibrotic liver tissues, which was accompanied by a significant inhibition of STAT3 phosphorylation. Moreover, we found that IL-17A stimulated the concentration-and time-dependent phosphorylation of STAT3 in AML-12 liver cells. Blocking STAT3 with a specific inhibitor STATTIC or STAT3 siRNA protected from the IL-17A-induced autophagy suppression in AML-12 cells, indicating that STAT3 mediates IL-17A-suppressed autophagy. Administration of IL-10, which activated STAT3 and inhibited autophagy, reversed the therapeutic effect of IL-17A antagonism in vivo. Our study suggests that the IL-17A/STAT3 signaling pathway plays a crucial role in the pathogenesis of hepatic fibrosis through suppressing hepatocellular autophagy and that blocking this pathway may provide therapeutic benefits for the treatment of hepatic 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.