ArticleFrontiers in medicine2026
ATF3 and HNF4A: an oxidative phosphorylation and cholesterol homeostasis-associated diagnostic and therapeutic repurposing framework target for metabolic dysfunction-associated steatohepatitis patients.
Article in Frontiers in medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Metabolic dysfunction-associated steatohepatitis (MASH) is hepatic steatosis. Oxidative phosphorylation and cholesterol homeostasis (OC) plays a key role in the onset and progression of MASH. Hence, deeper understanding of OC in MASH can shed light on the clinical applications for MASH patients. Methods: Metabolic dysfunction-associated steatohepatitis hepatic bulk profile (GSE89632) was subjected to GSVA and WGCNA analysis for identification of OC-associated highest correlated gene module and then intersected with OC-associated gene list downloaded from Genecard database for acquisition of OC-related DEGs. Next By integration of another MASH hepatic bulk profile (GSE164760) and machine learning algorithms (RF and Lasso) based on OC-associated DEGs, we identified hub variables. Next, OC-related diagnostic model based on hub variables was constructed on GSE164760 and then examined on the GSE89632 and GSE63067 (MASH bulk dataset). In addition, Consensus clustering was performed for the identification of OC-related molecular subgroups for MASH patient in GSE164760 and heterogeneity of hub variables was examined at MASH single-cell transcriptomic dataset (GSE189600) in temporal and spatial manners. DGIDB database with molecular docking and deep learning algorithm (Drugreflector) were performed for the identification of drug repurposing framework for reversing MASH to healthy status based on GSE164760 and potential agent targeting hub variables. Results: Activating Transcription Factor 3 and HNF4A were down-regulated and up-regulated expression hub variable associated with MASH pathogenesis, which illustrated satisfied diagnostic performance. ALVERINE and MECAMYLAMINE were potential therapeutic approaches for MASH treatment. Conclusion: Our study first indicated that OC was associated with MASH onset and progression, which can elaborate predictive and therapeutic potentials for MASH patients. Besides, ATF3 and HNF4A can be considered as OC-associated diagnostic and druggable targets for the treatment of MASH.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.