ReviewInternational journal of molecular sciences2023
Redox Biology and Liver Fibrosis.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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, 8 citations in OpenAlex.
- Hepatitis C Virus: An Overview of Its Chronic Impact on Liver Function, Metabolic Dysregulation, Inflammatory-Oxidative Pathogenesis and Epigenetic Memory.International journal of molecular sciences · 2026Review
- Metabolic Reprogramming Driven by Modifiable Lifestyle Factors in Metabolic Syndrome and Alcohol-Related Liver Disease: A Narrative Review.Metabolites · 2026Review
- Dioscin in liver diseases: pharmacological mechanisms, translational potential and future perspectives.Frontiers in pharmacology · 2026Review
- Congenital hepatic fibrosis and related ciliopathies across the life course: current management, disease burden, and unmet needs in the era of genomic diagnosis and translational therapeutics.Frontiers in pediatrics · 2026Review
- Molecular Imaging Probes for Early Detection and Staging of Liver Fibrosis.Chemical & biomedical imaging · 2025Review
- Association of cardiometabolic markers with hepatic steatosis and liver fibrosis in population without obesity and diabetes.Scientific reports · 2025Article
- Endothelial Dysfunction and Liver Cirrhosis: Unraveling of a Complex Relationship.International journal of molecular sciences · 2024Review
- Hovenia dulcis: a Chinese medicine that plays an essential role in alcohol-associated liver disease.Frontiers in pharmacology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic fibrosis is a complex process that develops in chronic liver diseases. Even though the initiation and progression of fibrosis rely on the underlying etiology, mutual mechanisms can be recognized and targeted for therapeutic purposes. Irrespective of the primary cause of liver disease, persistent damage to parenchymal cells triggers the overproduction of reactive species, with the consequent disruption of redox balance. Reactive species are important mediators for the homeostasis of both hepatocytes and non-parenchymal liver cells. Indeed, other than acting as cytotoxic agents, reactive species are able to modulate specific signaling pathways that may be relevant to hepatic fibrogenesis. After a brief introduction to redox biology and the mechanisms of fibrogenesis, this review aims to summarize the current evidence of the involvement of redox-dependent pathways in liver fibrosis and focuses on possible therapeutic targets.
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.