ArticleThe pharmacogenomics journal2020
A methylation functional detection hepatic cell system validates correlation between DNA methylation and drug-induced liver injury.
Article in The pharmacogenomics journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- Acetaminophen-induced acute liver injury abrogates the cytosine methylation pathway.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- Epigenetic Mechanisms Contribute to Intraindividual Variations of Drug Metabolism Mediated by Cytochrome P450 Enzymes.Drug metabolism and disposition: the biological fate of chemicals · 2023Review
- Human Cytochrome P450 1, 2, 3 Families as Pharmacogenes with Emphases on Their Antimalarial and Antituberculosis Drugs and Prevalent African Alleles.International journal of molecular sciences · 2023Review
- CRISPR/dCas9 for hepatic fibrosis therapy: implications and challenges.Molecular biology reports · 2022Review
- Differential effects on human cytochromes P450 by CRISPR/Cas9-induced genetic knockout of cytochrome P450 reductase and cytochrome b5 in HepaRG cells.Scientific reports · 2021Article
- Research Progress of Pharmacogenomics in Drug-Induced Liver Injury.Frontiers in pharmacology · 2021Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug-induced liver injury (DILI) is a life-threatening, adverse reaction to certain drugs. The onset and extent of DILI can vary drastically in different patients using identical drugs. Association studies suggested that subtle differences in DNA methylation may help explain the individual differences in DILI. However, there are very few experimental methods to confirm such associations. In this study, we established a novel DNA methylation functional detection system in human hepatocytes, using CRISPR/dCas9 for targeted modification of DNA methylation, and set four parameters to indicate the liver injury by cell model. Using this system, we validated the association of hypermethylation of CYP2D6 and CYP2E1 with rifampin-induced DILI. Our results revealed that, following treatment of HepaRG cells with rifampin, the methylation levels of CYP2D6 and CYP2E1 were inversely proportional to cell viability and glutathione content, and directly proportional to caspase 3/7 activity. We expect that our methylation detection system will serve as a useful tool in validating correlations between DNA methylation and DILI in other in vitro systems. Our results establish a foundation for future investigations to better understand the mechanisms underlying DILI and may aid in advancing personalized DILI medicine.
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Registered trials
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