ArticleGastroenterology2010
Modulation of hepatic fibrosis by c-Jun-N-terminal kinase inhibition.
Article in Gastroenterology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 120 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
120 citing papers in PubMed, 217 citations in OpenAlex.
- The autoregulatory feedback loop of microRNA-21/programmed cell death protein 4/activation protein-1 (MiR-21/PDCD4/AP-1) as a driving force for hepatic fibrosis development.The Journal of biological chemistry · 2013Trial
- Fatty Acid-Binding Proteins and Substance Use Disorders: From Lipid Signaling to Therapeutic Targets.Genes · 2026Review
- Glucolipid Metabolic Disorders andInternational journal of endocrinology · 2026Review
- Role of immunosuppressive JNK pathway in the tumor microenvironment among TNBC subtypes in IBCSG trial 22-00.iScience · 2025Article
- Antifibrotic therapies for metabolic dysfunction-associated steatotic liver disease.JHEP reports : innovation in hepatology · 2025Review
- Non-targeted metabolomics and network pharmacology of Taohong Siwu Decoction in hepatic fibrosis mouse model using high resolution mass spectrometry.Frontiers in molecular biosciences · 2025Article
- Quantitative Proteomic Study Reveals Amygdalin Alleviates Liver Fibrosis Through Inhibiting mTOR/PDCD4/JNK Pathway in Hepatic Stellate Cells.Drug design, development and therapy · 2025Article
- Hypoxia-Inducible Factor-2α Promotes Liver Fibrosis by Inducing Hepatocellular Death.International journal of molecular sciences · 2024Article
- Honey vesicle-like nanoparticles protect aged liver from non-alcoholic steatohepatitis.Acta pharmaceutica Sinica. B · 2024Article
- Liver Fibrosis: From Basic Science towards Clinical Progress, Focusing on the Central Role of Hepatic Stellate Cells.International journal of molecular sciences · 2024Review
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- Tenovin-1, a Selective SIRT1/2 Inhibitor, Attenuates High-fat Diet-induced Hepatic Fibrosis via Inhibition of HSC Activation in ZDF Rats.International journal of biological sciences · 2024Article
- JNKs protect from cholestatic liver disease progression by modulating Apelin signalling.JHEP reports : innovation in hepatology · 2023Article
- Non-alcoholic fatty liver disease: Immunological mechanisms and current treatments.World journal of gastroenterology · 2023Review
- Research Progress on the Role and Mechanism of IL-37 in Liver Diseases.Seminars in liver disease · 2023Article
- Impaired flux of bile acids from the liver to the gut reveals microbiome-immune interactions associated with liver damage.NPJ biofilms and microbiomes · 2023Article
- Identification of the c-Jun/H19/miR-19/JNK1 cascade during hepatic stellate cell activation.Clinical and translational medicine · 2023Article
- TREM2 Regulates the Removal of Apoptotic Cells and Inflammatory Processes during the Progression of NAFLD.Cells · 2023Article
- Linarin Protects Against CClDrug design, development and therapy · 2023Article
- Safety, Pharmacokinetics, and Pharmacodynamics of CC-90001 (BMS-986360), a c-Jun N-terminal Kinase Inhibitor, in Phase 1 Studies in Healthy Participants.Clinical pharmacology in drug development · 2022Article
60 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimsc-Jun N-terminal kinase (JNK) is activated by multiple profibrogenic mediators; JNK activation occurs during toxic, metabolic, and autoimmune liver injury. However, its role in hepatic fibrogenesis is unknown.
methodsJNK phosphorylation was detected by immunoblot analysis and confocal immunofluorescent microscopy in fibrotic livers from mice after bile duct ligation (BDL) or CCl(4) administration and in liver samples from patients with chronic hepatitis C and non-alcoholic steatohepatitis. Fibrogenesis was investigated in mice given the JNK inhibitor SP600125 and in JNK1- and JNK2-deficient mice following BDL or CCl(4) administration. Hepatic stellate cell (HSC) activation was determined in primary mouse HSCs incubated with pan-JNK inhibitors SP600125 and VIII.
resultsJNK phosphorylation was strongly increased in livers of mice following BDL or CCl(4) administration as well as in human fibrotic livers, occurring predominantly in myofibroblasts. In vitro, pan-JNK inhibitors prevented transforming growth factor (TGF) beta-, platelet-derived growth factor-, and angiotensin II-induced murine HSC activation and decreased platelet-derived growth factor and TGF-beta signaling in human HSCs. In vivo, pan-JNK inhibition did not affect liver injury but significantly reduced fibrosis after BDL or CCl(4). JNK1-deficient mice had decreased fibrosis after BDL or CCl(4), whereas JNK2-deficient mice displayed increased fibrosis after BDL but fibrosis was not changed after CCl(4). Moreover, patients with chronic hepatitis C who displayed decreased fibrosis in response to the angiotensin receptor type 1 blocker losartan showed decreased JNK phosphorylation.
conclusionsJNK is involved in HSC activation and fibrogenesis and represents a potential target for antifibrotic treatment approaches.
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What OpenQuestion holds
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.