ReviewGastroenterology2012
A liver full of JNK: signaling in regulation of cell function and disease pathogenesis, and clinical approaches.
Review in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 283 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
283 citing papers in PubMed, 1 synthesis or guideline pooled it, 483 citations in OpenAlex.
- Gene polymorphisms of inflammatory factors in liver cirrhosis.Frontiers in genetics · 2023Pooled it
- Hydrogen peroxide sensing and signaling in physiology and disease: implications for therapy.Signal transduction and targeted therapy · 2026Review
- Article
- Schisandrin B Targets the PPARγ-MAPK Signaling Axis to Ameliorate High-Fat MCD Diet-Induced MASLD in Mice.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Phospho-JNK agonists show promising effects for the treatment of hepatocellular carcinoma.iScience · 2026Article
- The E3 Ligase RNF8 Promotes Ubiquitination and Degradation of ChREBPα During Liver Stress Response.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- The bidirectional relationship between diabetes mellitus and liver disease: Mechanisms, clinical implications, and management strategies.Endocrine · 2026Review
- Diploid hepatocytes resist acetaminophen-induced liver injury through suppressed JNK signaling.Cell death & disease · 2026Article
- Therapeutic and Pharmacological Flexibility of Cinnamoyl Compounds: Targeting Multiple Signaling Pathways.Mini reviews in medicinal chemistry · 2026Review
- Vemurafenib Induces Apoptosis via JNK Activation and AKT Inhibition in Hepatocellular Carcinoma.Journal of Cancer · 2026Article
- Network pharmacology and molecular modelling analysis ofFrontiers in bioinformatics · 2026Article
- MicroRNA-21 is a potential therapeutic agent targetingMolecular therapy. Nucleic acids · 2025Article
- Quercetin and Its Metabolites: Mechanistic Insights as the Basis of Their Therapeutic Potential in NAFLD and HCC.Molecules (Basel, Switzerland) · 2025Review
- Endoplasmic reticulum stress at the forefront of fatty liver diseases and cancer.Pharmacological reviews · 2025Review
- Hepatoprotective Activity of Red Ginger Extract on Acetaminophen-induced Liver Injury Models in HepG2 Cells.Annals of African medicine · 2025Article
- Targeting Decidual Macrophage Polarization through JNK Signaling Pathway Inhibition Alleviates Adverse Pregnancy Outcomes in Early Spontaneous Abortion.Reproductive sciences (Thousand Oaks, Calif.) · 2025Article
- TGF-β/JNK axis mediates mitochondrial damage and macrophage cGAS-STING activation in liver Mallory-Denk body pathogenesis.Journal of translational medicine · 2025Article
- Role of C-Jun N-Terminal Kinases on a Stressed Epithelium: Time for Testing Isoform Specificity.Biology · 2025Review
- An association study ofBiochemistry and biophysics reports · 2025Article
- Mogroside V protects against acetaminophen-induced liver injury by reducing reactive oxygen species and c-jun-N-terminal kinase activation in mice.World journal of hepatology · 2025Article
223 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
3 authors at 1 institution in 1 country.
Funding
Abstract
c-Jun-N-terminal kinase (JNK) is a mitogen-activated protein kinase family member that is activated by diverse stimuli, including cytokines (such as tumor necrosis factor and interleukin-1), reactive oxygen species (ROS), pathogens, toxins, drugs, endoplasmic reticulum stress, free fatty acids, and metabolic changes. Upon activation, JNK induces multiple biologic events through the transcription factor activator protein-1 and transcription-independent control of effector molecules. JNK isozymes regulate cell death and survival, differentiation, proliferation, ROS accumulation, metabolism, insulin signaling, and carcinogenesis in the liver. The biologic functions of JNK are isoform, cell type, and context dependent. Recent studies using genetically engineered mice showed that loss or hyperactivation of the JNK pathway contributes to the development of inflammation, fibrosis, cancer growth, and metabolic diseases that include obesity, hepatic steatosis, and insulin resistance. We review the functions and pathways of JNK in liver physiology and pathology and discuss findings from preclinical studies with JNK inhibitors.
Indexed as
Identifiers
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.