Animal models of drug-induced liver injury

被引:137
作者
McGill, Mitchell R. [1 ,2 ]
Jaeschke, Hartmut [3 ]
机构
[1] Univ Arkansas Med Sci, Fay W Boozman Coll Publ Hlth, Dept Environm & Occupat Hlth, Little Rock, AR 72205 USA
[2] Univ Arkansas Med Sci, Coll Med, Dept Pharmacol & Toxicol, Little Rock, AR 72205 USA
[3] Univ Kansas, Med Ctr, Dept Pharmacol Toxicol & Therapeut, 3901 Rainbow Blvd,MS1018, Kansas City, KS 66160 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2019年 / 1865卷 / 05期
基金
美国国家卫生研究院;
关键词
Acetaminophen; Carbon tetrachloride; Intrinsic hepatotoxicity; Idiosyncratic hepatotoxicity; Immune tolerance; ACETAMINOPHEN-PROTEIN ADDUCTS; N-TERMINAL KINASE; INDUCED HEPATIC-NECROSIS; INHIBITING CYTOCHROME-P450 ENZYMES; NEUTROPHIL DEPLETION PROTECTS; CARBON-TETRACHLORIDE; MITOCHONDRIAL DYSFUNCTION; CELL-DEATH; INDUCED HEPATOTOXICITY; MOUSE MODEL;
D O I
10.1016/j.bbadis.2018.08.037
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Drug-induced liver injury (DILI) presents unique challenges for consumers, clinicians, and regulators. It is the most common cause of acute liver failure in the US. It is also one of the most common reasons for termination of new drugs during pre-clinical testing and withdrawal of new drugs post-marketing. DILI is generally divided into two forms: intrinsic and idiosyncratic. Many of the challenges with DILI are due in large part to poor understanding of the mechanisms of toxicity. Although useful models of intrinsic DILI are available, they are frequently misused. Modeling idiosyncratic DILI presents greater challenges, but promising new models have recently been developed. The purpose of this manuscript is to provide a critical review of the most popular animal models of DILI, and to discuss the future of DILI research.
引用
收藏
页码:1031 / 1039
页数:9
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