ReviewTrends in endocrinology and metabolism: TEM2026
Mechanisms and therapeutic insights into MASH-associated fibrosis.
Review in Trends in endocrinology and metabolism: TEM, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Cardiovascular Disease in the Context of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A Comprehensive Narrative Review.International journal of molecular sciences · 2025Pooled it
- Article
- Obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A Literature Review on Pathophysiology and Treatment.Diabetes, obesity & metabolism · 2026Review
- Review
- Immune Determinants of MASLD Progression: From Immunometabolic Reprogramming to Fibrotic Transformation.Biology · 2026Review
- Metabolic dysfunction-associated steatotic liver disease and heart failure with preserved ejection fraction: mechanisms and clinical implications from a heart-liver metabolic axis perspective.Frontiers in pharmacology · 2026Review
- Loss of immunometabolic adaptability in MASH: gut-derived signals drive macrophage reprogramming and fibrosis.Frontiers in immunology · 2026Review
- Decoding the heterogeneity of liver-resident macrophages in chronic liver diseases: therapeutic responses to immunomodulatory strategies.Frontiers in pharmacology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Metabolic dysfunction-associated steatohepatitis (MASH) is a progressive liver disease posing a major global health concern, closely related to the rising prevalence of obesity. Liver fibrosis is the primary determinant of adverse outcomes in MASH. The increasing worldwide prevalence, economic impact, and adverse outcomes of MASH-associated fibrosis have spurred extensive research to elucidate its pathogenesis and to address its treatment. However, the intricate mechanism driving the transition from metabolic dysfunction to clinically significant fibrosis is not fully understood. Moreover, effective therapies, particularly direct antifibrotic agents, are still lacking, despite the recent approval of resmetirom and semaglutide for MASH-associated fibrosis. Here, we review current insights into the mechanism of MASH-associated fibrosis and provide a comprehensive overview of emerging therapeutic strategies.
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.