A mini-review of the rodent models for alcoholic liver disease: Shortcomings, application, and future prospects
Toxicology Research, ISSN: 2045-4538, Vol: 10, Issue: 3, Page: 523-530
2021
- 17Citations
- 4Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations17
- Citation Indexes17
- 17
- Captures4
- Readers4
Review Description
Rodents are the most common models in studies of alcoholic liver disease (ALD). Although several rodents ALD models have been established and multiple mechanisms have been elucidated based on them, these models have some non-negligible shortcomings, specifically only inducing early stage (mainly steatosis, slight to moderate steatohepatitis) but not the whole spectrum of human ALD. The resistance of rodents to advanced ALD has been suggested to be due to the physiological differences between rodents and human beings. Previous studies have reported significant interstrain differences in the susceptibility to ethanol-induced liver injury and in the manifestation of ALD (such as different alteration of lipid profiles). Therefore, it would be interesting to characterize the manifestation of ethanol-induced liver damage in various rodents, which may provide a recommendation to investigators of ALD. Furthermore, more severe ALD models need to be established for the study of serious ALD forms, which may be achieved by using genetic modified rodents.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85111798220&origin=inward; http://dx.doi.org/10.1093/toxres/tfab042; http://www.ncbi.nlm.nih.gov/pubmed/34141166; https://academic.oup.com/toxres/article/10/3/523/6272659; https://dx.doi.org/10.1093/toxres/tfab042; https://academic.oup.com/toxres/article-abstract/10/3/523/6272659?redirectedFrom=fulltext
Oxford University Press (OUP)
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