ArticleVeterinary research
Signaling pathways involved in liver injury and regeneration in rabbit hemorrhagic disease, an animal model of virally-induced fulminant hepatic failure.
Article in Veterinary research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- Molecular and Regenerative Effects of Platelet-Rich Plasma and Related Hemocomponents in Animal Models of Liver Injury-A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Rabbit hemorrhagic disease: The devastating impact of a highly contagious virus on rabbit populations.Open veterinary journal · 2025Review
- MicroRNAs Regulate the Expression of Genes Related to the Innate Immune and Inflammatory Response in Rabbits Infected withInternational journal of molecular sciences · 2024Article
- Apoptotic Cell Death in an Animal Model of Virus-Induced Acute Liver Failure-Observations duringInternational journal of molecular sciences · 2024Article
- MicroRNAs participate in the regulation of apoptosis and oxidative stress-related gene expression in rabbits infected withFrontiers in microbiology · 2024Article
- Crosstalk between Apoptosis and Cytotoxic Lymphocytes (CTLs) in the Course ofJournal of veterinary research · 2023Article
- Apoptosis activation duringFrontiers in microbiology · 2023Article
- Immunity againstVaccines · 2021Review
- Article
- Crocetin Improves Dengue Virus-Induced Liver Injury.Viruses · 2020Article
- Melatonin modulates mitophagy, innate immunity and circadian clocks in a model of viral-induced fulminant hepatic failure.Journal of cellular and molecular medicine · 2020Article
- Rabbit Hemorrhagic Disease Virus Non-structural Protein 6 Induces Apoptosis in Rabbit Kidney Cells.Frontiers in microbiology · 2018Article
- Autophagic response in the Rabbit Hemorrhagic Disease, an animal model of virally-induced fulminant hepatic failure.Veterinary research · 2014Article
- Immunosuppression abrogates resistance of young rabbits to Rabbit Haemorrhagic Disease (RHD).Veterinary research · 2014Article
- Allopurinol ameliorates thioacetamide-induced acute liver failure by regulating cellular redox-sensitive transcription factors in rats.Inflammation · 2012Article
- Rabbit haemorrhagic disease (RHD) and rabbit haemorrhagic disease virus (RHDV): a review.Veterinary research · 2012Review
- Cardiotrophin-1 promotes a high survival rate in rabbits with lethal fulminant hepatitis of viral origin.Journal of virology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Management of fulminant hepatic failure (FHF) continues to be one challenging problem, and experimental animal models resembling its clinical conditions are still needed. Rabbit hemorrhagic disease (RHD) fullfils many requirements of an animal model of FHF. This work investigated changes in MAPK, NF-kappaB, AP-1 and STAT pathways during RHD-induced liver injury. Rabbits were infected with 2 x 10(4) hemagglutination units of an RHD virus isolate. Apoptosis was documented by the presence of caspase-3 activity and substantial PARP proteolysis at 36 and 48 h postinfection (pi). Infection induced a marked and maintained expression of TNF-alpha from 12 h pi, while there was only a transitory increase in IL-6 expression. Expression of phosphorylated (p)-JNK, p-p38 and p-ERK1/2 was significantly elevated at 12 h pi. At 48 h pi p-JNK expression was maintained at a maximum level, while that of p-p38 returned to normality and there was no p-ERK1/2 expression. Activation of NF-kappaB and AP-1 and increased expression of VCAM-1 and COX-2 were observed. No significant changes were detected in activation of STAT1 and STAT3, while SOCS3 expression increased significantly. The current findings suggest that activation of JNK is an essential component in liver injury mediated by the RHD virus and that lack of activation of STAT3, probably mediated by SOCS3 over-expression, would contribute to the inhibition of the regenerative response. Data show the presence of molecular mechanisms contributing to liver damage and the lack of regeneration and they support the usefulness of this model to investigate novel therapeutical modalities in FHF.
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.