ReviewMetabolites2024
Endpoints in NASH Clinical Trials: Are We Blind in One Eye?
Review in Metabolites, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 28 citations in OpenAlex.
- Clinical trial endpoints for metabolic dysfunction and alcohol associated steatotic liver disease.Hepatology international · 2026Review
- Efficacy of Orlistat on Cardiometabolic Indices in Patients With Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A GRADE-Assessed Systematic Review and Meta-Analysis of RCTs.Current therapeutic research, clinical and experimental · 2026Review
- Irisin alleviates hepatic steatosis by activating the autophagic SIRT3 pathway.Chinese medical journal · 2026Article
- Empagliflozin attenuates dexamethasone-induced non-alcoholic steatohepatitis by regulation of ferroptosis, inflammation and autophagy.Frontiers in pharmacology · 2026Article
- The immunometabolic mechanisms and therapeutic targets of metabolic dysfunction-associated steatohepatitis.Frontiers in medicine · 2026Review
- Sex Hormones and Metabolic Dysfunction-Associated Steatotic Liver Disease.International journal of molecular sciences · 2025Review
- Lifestyle Intervention Improves Metabolic Dysfunction-Associated Steatotic Liver Disease in Children with Down Syndrome.Nutrients · 2025Article
- Red cell distribution width/platelet ratio predicts decompensation of metabolic dysfunction-associated steatotic liver disease-related compensated advanced chronic liver disease.World journal of gastroenterology · 2025Article
- Exploring drug repurposing as a therapeutic strategy for non-alcoholic fatty liver disease (NAFLD): identification of potential targets and pathways.Gastroenterology and hepatology from bed to bench · 2025Article
- Molecular Pharmacology of Vitamin C and Relevance to Health and Obesity-A Narrative Review.International journal of molecular sciences · 2024Review
- Does an Aspirin a Day Take the MASLD Away?Advances in therapy · 2024Review
- Alanine aminotransferase predicts incident steatotic liver disease of metabolic etiology: Long life to the old biomarker!World journal of gastroenterology · 2024Article
- Advancements in pharmacological treatment of NAFLD/MASLD: a focus on metabolic and liver-targeted interventions.Gastroenterology report · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This narrative review aims to illustrate the notion that nonalcoholic steatohepatitis (NASH), recently renamed metabolic dysfunction-associated steatohepatitis (MASH), is a systemic metabolic disorder featuring both adverse hepatic and extrahepatic outcomes. In recent years, several NASH trials have failed to identify effective pharmacological treatments and, therefore, lifestyle changes are the cornerstone of therapy for NASH. with this context, we analyze the epidemiological burden of NASH and the possible pathogenetic factors involved. These include genetic factors, insulin resistance, lipotoxicity, immuno-thrombosis, oxidative stress, reprogramming of hepatic metabolism, and hypoxia, all of which eventually culminate in low-grade chronic inflammation and increased risk of fibrosis progression. The possible explanations underlying the failure of NASH trials are also accurately examined. We conclude that the high heterogeneity of NASH, resulting from variable genetic backgrounds, exposure, and responses to different metabolic stresses, susceptibility to hepatocyte lipotoxicity, and differences in repair-response, calls for personalized medicine approaches involving research on noninvasive biomarkers. Future NASH trials should aim at achieving a complete assessment of systemic determinants, modifiers, and correlates of NASH, thus adopting a more holistic and unbiased approach, notably including cardiovascular-kidney-metabolic outcomes, without restricting therapeutic perspectives to histological surrogates of liver-related outcomes alone.
Indexed as
Identifiers
What 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.