Trial reportClinical epigenetics2025
HCV patients with residual fibrosis after DAA treatment re-establish their epigenetic signature after prolonged-release pirfenidone: MINERVA study.
Trial report in Clinical epigenetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05542615 (Evaluation of Prolonged-release Pirfenidone in Patients With Viral C Hepatitis, With Sustained Viral Response and Advanced Residual Liver Fibrosis. Potential Role of Epigenetics to Understand Therapeutic Changes), which is not on this map. Cited by 1 paper.
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.
Evaluation of Prolonged-release Pirfenidone in Patients With Viral C Hepatitis, With Sustained Viral Response and Advanced Residual Liver Fibrosis. Potential Role of Epigenetics to Understand Therapeutic Changes (MINERVA).
Who cites it
1 citing paper in PubMed.
- Pirfenidone Sensitizes Hepatic Stellate Cells to Ferroptosis by Reprogramming Glutamine and Serine Metabolism for GSH Depletion.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
BACKGROUND &
aimsPatients with residual liver fibrosis after hepatitis C virus infection clearance represent an important challenge. The primary objective of this study was to evaluate epigenetic marks in DAA-responders HCV, Hispanic patients with remaining fibrosis who were treated with prolonged-release pirfenidone (PR-PFD).
methodsForty-four DAA-responders HCV patients presenting remaining fibrosis received PR-PFD (1200 mg/day) for 12 months. Liver biopsies and serum samples were analyzed. Patients were classified as regressive fibrotic profile (RFP), stable fibrosis profile (SFP), or progressive fibrotic profile (PFP) based on liver stiffness (Fibroscan) (± 30% variation). A control cohort of 20 DAA-responders HCV patients received only standard of care treatment. Additionally, six non-fibrotic controls were included to compare epigenetic marks.
resultsThirty-eight patients completed the 12-month treatment; 28.94% showed a reduction in at least one fibrosis stage based on liver biopsies. Fibroscan revealed that 44.73% of patients in the PR-PFD group exhibited RFP. Bilirubin, alkaline phosphatase, AST, INR and APRI values significantly decreased in this group. Noteworthy, 85% of 20 control patients had SFP. Profibrogenic miRNAs displayed a significant increase in expression in advanced fibrosis versus controls without fibrosis. PR-PFD treatment restored the expression of miR-34a, miR-16, miR-192, miR-200a, and miR-122. PDGFA CpGs hypermethylation in both cell-free DNA and liver biopsies has been found in advanced fibrosis. Interestingly, four CpGs in PPARD were hypomethylated compared to controls. PR-PFD treatment resulted in hypermethylation of three TGFB1-CpGs.
conclusionThese findings indicate for the first time that PR-PFD might exert therapeutic effects in Hispanic patients with residual fibrosis by modulating the expression of miRNAs and methylation of specific CpG sites. CLINICAL TRIAL NUMBER: NCT05542615. Registration Date 09/13/2022.
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