ReviewEpigenomics2026
Epigenetic regulation in MASLD - insight for therapeutic target discovery.
Review in Epigenomics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease. It encompasses metabolic affections that arise primarily from lifestyle and diet, independent of alcohol consumption. Particularly, the global rise in obesity constitutes a major risk factor and comorbidity, contributing to the prevalence and severity of MASLD. Despite its widespread impact and potential progression to severe liver pathologies, effective therapies remain limited, underscoring the urgency to better understand its underlying molecular mechanisms.Epigenetic regulation is essential for maintaining hepatic metabolic function and cellular identity in response to metabolic cues but becomes critically dysregulated during MASLD. Alterations in DNA methylation, histone modifications, and non-coding RNAs contribute to disease progression, promoting metabolic dysfunction and lipid accumulation. Recent evidence indicates that epigenetic dysregulation in MASLD also occurs in a spatial manner where changes in chromatin accessibility, zone-enriched microRNAs, and transcription factor activity can disrupt gene expression along the periportal-pericentral axis, leading to zone-specific disturbances in metabolic specialization, which emerges as a critical novel factor influencing the onset and progression of MASLD. Furthermore, this review explores the role of microRNAs and extracellular vesicles in mediating systemic metabolic dysfunction observed in MASLD and highlights emerging epigenetic strategies with therapeutic potential in MASLD.
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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 Socratic graph.