Trial reportAmerican journal of physiology. Gastrointestinal and liver physiology2009
Effects of losartan on hepatic expression of nonphagocytic NADPH oxidase and fibrogenic genes in patients with chronic hepatitis C.
Trial report in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Therapeutic effect of renin angiotensin system inhibitors on liver fibrosis.Journal of the renin-angiotensin-aldosterone system : JRAASPooled it
- Role of extracellular matrix in liver fibrosis regression and regeneration (Review).International journal of molecular medicine · 2026Review
- Human endogenous retrovirus W family envelope protein (ERVWE1) regulates macroautophagy activation and micromitophagy inhibition via NOXA1 in schizophrenia.Virologica Sinica · 2025Article
- Mechanism-guided drug development and treatment for liver fibrosis: a clinical perspective.Frontiers in pharmacology · 2025Review
- Endotoxemia and Gastrointestinal Cancers: Insight into the Mechanisms Underlying a Dangerous Relationship.Microorganisms · 2023Review
- NOX as a Therapeutic Target in Liver Disease.Antioxidants (Basel, Switzerland) · 2022Review
- Quantitative Susceptibility Mapping versus R2*-based Histogram Analysis for Evaluating Liver Fibrosis: Preliminary Results.Magnetic resonance in medical sciences : MRMS : an official journal of Japan Society of Magnetic Resonance in Medicine · 2022Article
- Review
- Review
- Molecular Mechanisms and Potential New Therapeutic Drugs for Liver Fibrosis.Frontiers in pharmacology · 2022Review
- Therapeutic and diagnostic targeting of fibrosis in metabolic, proliferative and viral disorders.Advanced drug delivery reviews · 2021Review
- COVID-19, ferrosenescence and neurodegeneration, a mini-review.Progress in neuro-psychopharmacology & biological psychiatry · 2021Review
- Synergistic effects of sitagliptin and losartan against fipronil-induced hepatotoxicity in rats.Veterinary world · 2021Article
- Liver Disease: Induction, Progression, Immunological Mechanisms, and Therapeutic Interventions.International journal of molecular sciences · 2021Review
- Review
- Liver Fibrosis: Therapeutic Targets and Advances in Drug Therapy.Frontiers in cell and developmental biology · 2021Review
- Efficacy and safety of anti-hepatic fibrosis drugs.World journal of gastroenterology · 2020Review
- Review
- "Let my liver rather heat with wine" - a review of hepatic fibrosis pathophysiology and emerging therapeutics.Hepatic medicine : evidence and research · 2019Article
- Role of the renin-angiotensin system in hepatic fibrosis and portal hypertension.The Korean journal of internal medicine · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Angiotensin II promotes liver fibrogenesis by stimulating nonphagocytic NADPH oxidase (NOX)-induced oxidative stress. Angiotensin II type 1 (AT1) receptor blockers attenuate experimental liver fibrosis, yet their effects in human liver fibrosis are unknown. We investigated the effects of losartan on hepatic expression of fibrogenic, inflammatory, and NOX genes in patients with chronic hepatitis C (CHC). Fourteen patients with CHC and liver fibrosis received oral losartan (50 mg/day) for 18 mo. Liver biopsies were performed at baseline and after treatment. The degree of inflammation and fibrosis was evaluated by histological analysis (METAVIR). Collagen content was measured by morphometric quantification of Sirius red staining. Overall collagen content and fibrosis stage remained stable in the whole series, yet the fibrosis stage decreased in seven patients. Inflammatory activity improved in seven patients. The effect of losartan on hepatic expression of 31 profibrogenic and inflammatory genes and components of the NOX complex was assessed by quantitative PCR. Losartan treatment was associated with a significant decrease in the expression of several profibrogenic and NOX genes including procollagen alpha1(I) and alpha1(IV), urokinase-type plasminogen activator, metalloproteinase type 2, NOX activator 1 (NOXA-1) and organizer 1 (NOXO-1), and Rac-1. Losartan was well tolerated in all patients and was effective in attenuating the activity of the systemic renin-angiotensin system. No effects on serum liver tests or viral load were observed. We conclude that prolonged administration of losartan, an oral AT1 receptor blocker, is associated with downregulation of NOX components and fibrogenic genes in patients with CHC. Controlled studies are warranted to assess the effect of AT1 receptor blockers in chronic liver injury.
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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.