ReviewJournal of hepatology2023
An integrated view of anti-inflammatory and antifibrotic targets for the treatment of NASH.
Review in Journal of hepatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 2 of them syntheses 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
175 citing papers in PubMed, 2 syntheses or guidelines pooled it, 270 citations in OpenAlex.
- Lingguizhugan Decoction in the Treatment of Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis.Endocrine, metabolic & immune disorders drug targets · 2025Pooled it
- Crosstalk between fibroblasts and immunocytes in fibrosis: From molecular mechanisms to clinical trials.Clinical and translational medicine · 2024Pooled it
- The liver in diabetes: current state and future perspectives.Diabetologia · 2026Review
- Hepatic fibrosis extracellular matrix stiffness induces abnormal maturation of dendritic cell via AMPK inhibition-mediated cholesterol accumulation.Materials today. Bio · 2026Article
- Review
- Reconstructing AF-associated atrial fibrosis: Patient-specific iPSC models, fit-for-purpose atrial microphysiological systems, and nanomedicine.Materials today. Bio · 2026Review
- A Conserved Macrophage-to-Hepatic Stellate Cell PDGF Axis in Human MASH Identified by Multi-Cohort sc/snRNA-Seq Re-Analysis.International journal of molecular sciences · 2026Article
- Review
- Free Fatty acid-induced disruption of hepatic vitamin D metabolism impairs bone homeostasis in an in vitro 3D human liver-bone model.Archives of toxicology · 2026Article
- GLP-1 receptor agonists in metabolic dysfunction-associated steatotic liver disease: mechanistic networks and translational implications: a review.Journal of endocrinological investigation · 2026Review
- Plant-Derived Exosome-like Nanovesicles for Metabolic Dysfunction-Associated Steatotic Liver Disease.Veterinary sciences · 2026Review
- With no lysine kinase 1 in hepatic stellate cells promotes mouse and human liver fibrosis through glycolytic triosephosphate isomerase 1.Hepatology (Baltimore, Md.) · 2026Article
- Engineering oral celastrol-polysaccharide supramolecular nanoassemblies across intestinal barriers for the intervention of nonalcoholic steatohepatitis.Materials today. Bio · 2026Article
- Drug Development for MASH-Related Compensated Cirrhosis: Past, Present and Future.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- GLP-1 Mitigated Inflammation and Oxidative Stress in Oral Lichen Planus Via JAK-STAT3 Pathway.Biochemical genetics · 2026Article
- Reprogramming macrophages to treat liver diseases.Hepatology (Baltimore, Md.) · 2026Review
- Alteration of small intestinal microbiota in diet-induced steatohepatitis mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Epigenetically controlled endothelial promyelocytic leukemia drives liver inflammation and fibrosis.The Journal of clinical investigation · 2026Article
- From bench to bedside: Molecular mechanisms, diagnostic tools, and therapeutic strategies in liver fibrosis.Liver research (Beijing, China) · 2026Review
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
115 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
Successful development of treatments for non-alcoholic fatty liver disease and its progressive form, non-alcoholic steatohepatitis (NASH), has been challenging. Because NASH and fibrosis lead to progression towards cirrhosis and clinical outcomes, approaches have either sought to attenuate metabolic dysregulation and cell injury, or directly target the inflammation and fibrosis that ensue. Targets for reducing the activation of inflammatory cascades include nuclear receptor agonists (e.g. resmetirom, lanifibranor, obeticholic acid), modulators of lipotoxicity (e.g. aramchol, acetyl-CoA carboxylase inhibitors) or modification of genetic variants (e.g. PNPLA3 gene silencing). Extrahepatic inflammatory signals from the circulation, adipose tissue or gut are targets of hormonal agonists (semaglutide, tirzepatide, FGF19/FGF21 analogues), microbiota or lifestyle interventions. Stress signals and hepatocyte death activate immune responses, engaging innate (macrophages, innate lymphocyte populations) and adaptive (auto-aggressive T cells) mechanisms. Therapies have also been developed to blunt immune cell activation, recruitment (chemokine receptor inhibitors), and responses (e.g. galectin-3 inhibitors, anti-platelet drugs). The disease-driving pathways of NASH converge to elicit fibrosis, which is reversible. The activation of hepatic stellate cells into matrix-producing myofibroblasts can be inhibited by antagonising soluble factors (e.g. integrins, cytokines), cellular crosstalk (e.g. with macrophages), and agonising nuclear receptor signalling. In advanced fibrosis, cell therapy with restorative macrophages or reprogrammed (CAR) T cells may accelerate repair through hepatic stellate cell deactivation or killing, or by enhancing matrix degradation. Heterogeneity of disease - either due to genetics or divergent disease drivers - is an obstacle to defining effective drugs for all patients with NASH that will be overcome incrementally.
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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.