ReviewNature reviews. Drug discovery2025
Therapeutic landscape of metabolic dysfunction-associated steatohepatitis (MASH).
Review in Nature reviews. Drug discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Sarcopenia as a risk factor for nonalcoholic fatty liver disease and liver fibrosis: an updated systematic review and meta-analysis.Frontiers in nutrition · 2026Pooled it
- Targeting ROAM1 with UDP-GlcNAc nanosheets selective activates lysosomal AMPK to resolve metabolic dysfunction-associated steatotic liver disease.Bioactive materials · 2026Article
- GLP-1 receptor agonists in metabolic dysfunction-associated steatohepatitis: a systematic review and meta-analysis of randomized controlled trials.Hepatology international · 2026Article
- Gut-Liver Translocation of Bacteroides Uniformis Alleviates Advanced Metabolic Dysfunction-Associated Steatotic Liver Disease by Suppressing Hepatocyte Ferroptosis via Propionic Acid Secretion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- First-in-Human Dose Selection, Pharmacokinetics Prediction, and Clinical Validation of SYHA1805, a Novel FXR Agonist, Using Allometric Scaling and PBPK Modeling.Pharmaceutics · 2026Article
- Liver fibrosis in metabolic dysfunction-associated steatotic liver disease: epidemiology, risk stratification and therapeutics.BMJ open gastroenterology · 2026Review
- Letter to the editor on "Evaluating treatment response thresholds for cost-effective treatment in metabolic dysfunction-associated steatotic liver disease".Clinical and molecular hepatology · 2026Article
- Role of LncSNHG5 in MAFLD: Mechanisms of Arid1a K391 lactylation and lipid accumulation.Clinical and translational medicine · 2026Article
- Integrative Multi-Omics Analysis Elucidates the Progressive Disease Landscape and Reveals Dynamic Protein Biomarkers for MASLD Surveillance.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Regional Inequities in Metabolic Dysfunction-associated Steatotic Liver Disease Burden and Care Quality in High-burden Settings: Implications for Health Systems.Journal of clinical and translational hepatology · 2026Article
- Novel bile salt analogs reduce lipid accumulation in liver cells with potential to treat both metabolic dysfunction-associated steatotic liver disease and Clostridioides difficile infection.bioRxiv : the preprint server for biology · 2026Article
- Review
- Germline mutations and somatic mosaicism in steatotic liver diseases and related liver carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2026Review
- The versatile interplay between steatotic liver disease and liver cancer.Nature reviews. Cancer · 2026Review
- Dyslipidemias associated with endocrine disorders: a position statement of the working group of the nutrition hormones and metabolism club of the italian society of endocrinology (SIE).Journal of endocrinological investigation · 2026Article
- RYK is a GPNMB receptor that drives MASH.Nature · 2026Article
- Selenoprotein H Functions as a PPARα Coactivator to Link Selenium Homeostasis to Hepatic Lipid Metabolism and Protect against Steatohepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Liver Stiffness Rises Early in MASLD and Drives Inflammation, Lipid Dysmetabolism, and Fibrosis via Piezo1-YAP Mechanotransduction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- GLP-1RA may open a new era for MASLD treatment: Editorial on "Glucagon-like peptide 1 receptor agonist and reduced liver and non-liver complications in adults with type 2 diabetes and metabolic dysfunction-associated steatotic liver disease: a target trial emulation study".Clinical and molecular hepatology · 2026Article
- Macrophage β-catenin-Ihh axis induces hepatic stellate cell activation and fibrosis in metabolic dysfunction-associated steatohepatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
16 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) and its severe subgroup metabolic dysfunction-associated steatohepatitis (MASH) have become a global epidemic and are driven by chronic overnutrition and multiple genetic susceptibility factors. The physiological outcomes include hepatocyte death, liver inflammation and cirrhosis. The first therapeutic for MASLD and MASH, resmetirom, has recently been approved for clinical use and has energized this therapeutic space. However, there is still much to learn in clinical studies of MASH, such as the scale of placebo responses, optimal trial end points, the time required for fibrosis reversal and side effect profiles. This Review introduces aspects of disease pathogenesis related to drug development and discusses two main therapeutic approaches. Thyroid hormone receptor-β agonists, such as resmetirom, as well as fatty acid synthase inhibitors, target the liver and enable it to function within a toxic metabolic environment. In parallel, incretin analogues such as semaglutide improve metabolism, allowing the liver to self-regulate and reversing many aspects of MASH. We also discuss how combinations of therapeutics could potentially be used to treat patients.
Indexed as
Identifiers
39609545What Socratic 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 Socratic graph.