ReviewThe Journal of clinical investigation2025
MASH: the nexus of metabolism, inflammation, and fibrosis.
Review in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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
55 citing papers in PubMed.
- Liver fibrosis: Pathogenesis and innovative nanoparticle-based therapeutic strategies.International journal of pharmaceutics: X · 2026Review
- Metabolic drivers of MASLD and MASH: from hormonal imbalance to fibrosis.Diabetologia · 2026Review
- Review
- E3 Ubiquitin Ligases in MASH-Associated Liver Fibrosis: Mechanisms and Therapeutic Opportunities.Liver international : official journal of the International Association for the Study of the Liver · 2026Review
- Clinical trials in a dish: cardiometabolic drug development with biological and digital twins.The Journal of clinical investigation · 2026Review
- FBP1-Mediated Compartmentalization of Glycolytic Enzyme Complexes Suppresses PKM2 Function to Ameliorate MASLD Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chronic Dietary Stress Is Associated with Early Cardiac Dysfunction and Progressive MASH Accompanied by Systemic Inflammation and Fibrosis.Nutrients · 2026Article
- Betaine in Metabolic Dysfunction-Associated Steatotic Liver Disease: Mechanisms of Action and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2026Review
- Nutriomic Technologies for Characterizing, Diagnosing, Clustering and Managing Chronic Liver Diseases: Precision Nutrition Implications.International journal of molecular sciences · 2026Review
- Article
- Proteomic Analysis of Retinas from Two Different Type-1 Diabetic Models.Biomolecules · 2026Article
- From metabolites to membrane vesicles: Unifying gut microbial signals in obesity, t2dm, and MASLD.World journal of microbiology & biotechnology · 2026Review
- Korean red ginseng saponins ameliorate metabolic dysfunction-associated steatohepatitis in mice by inhibiting caspase-11 and NLRP3 inflammasomes.Journal of ginseng research · 2026Article
- Retrospective analysis of platelet to high-density lipoprotein cholesterol ratio in obese children with metabolic dysfunction-associated fatty liver disease.Translational pediatrics · 2026Article
- The Effect of Prolyl Isomerase Pin1 on the Development of Metabolic Dysfunction-Associated Steatohepatitis and a New Treatment Strategy.International journal of molecular sciences · 2026Review
- Pathogenesis-Informed Phenotype-Guided Therapy for MASH: A Three-Axis Translational Framework Within the MASLD Spectrum.Biomedicines · 2026Review
- [Mesenchymal stem cell-derived exosomes: a new hope for metabolic-associated fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026Review
- Determinants of Metabolic Dysfunction-Associated Steatotic Liver Diseases in Patients with Type 2 Diabetes Mellitus.Journal of clinical medicine · 2026Article
- Network Pharmacology and In Vivo Validation Reveal Berberine-Mediated Regulation of the Liver-Brain Inflammatory Axis in MCD-Induced Steatohepatitis.International journal of molecular sciences · 2026Article
- Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive form of liver disease characterized by hepatocyte injury, inflammation, and fibrosis. The transition from metabolic dysfunction-associated steatotic liver disease (MASLD) to MASH is driven by the accumulation of toxic lipid and metabolic intermediates resulting from increased hepatic uptake of fatty acids, elevated de novo lipogenesis, and impaired mitochondrial oxidation. These changes promote hepatocyte stress and cell death, activate macrophages, and induce a fibrogenic phenotype in hepatic stellate cells (HSCs). Key metabolites, including saturated fatty acids, free cholesterol, ceramides, lactate, and succinate, act as paracrine signals that reinforce inflammatory and fibrotic responses across multiple liver cell types. Crosstalk between hepatocytes, macrophages, and HSCs, along with spatial shifts in mitochondrial activity, creates a feed-forward cycle of immune activation and tissue remodeling. Systemic inputs, such as insulin-resistant adipose tissue and impaired clearance of dietary lipids and branched-chain amino acids, further contribute to liver injury. Together, these pathways establish a metabolically driven network linking nutrient excess to chronic liver inflammation and fibrosis. This Review outlines how coordinated disruptions in lipid metabolism and intercellular signaling drive MASH pathogenesis and provides a framework for understanding disease progression across tissue and cellular compartments.
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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.