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Troglitazone hepatotoxicity: are we getting closer to understanding idiosyncratic liver injury?

作者信息

Jaeschke Hartmut

机构信息

Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, MS 1018, Kansas City, Kansas 66160, USA.

出版信息

Toxicol Sci. 2007 May;97(1):1-3. doi: 10.1093/toxsci/kfm021.

DOI:10.1093/toxsci/kfm021
PMID:17575588
Abstract
摘要

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Troglitazone hepatotoxicity: are we getting closer to understanding idiosyncratic liver injury?曲格列酮肝毒性：我们离理解特异质性肝损伤更近了吗？
Toxicol Sci. 2007 May;97(1):1-3. doi: 10.1093/toxsci/kfm021.
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Troglitazone-induced hepatic necrosis in an animal model of silent genetic mitochondrial abnormalities.曲格列酮在隐匿性遗传性线粒体异常动物模型中诱导肝坏死。
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The mitochondrial superoxide/thioredoxin-2/Ask1 signaling pathway is critically involved in troglitazone-induced cell injury to human hepatocytes.线粒体超氧化物/硫氧还蛋白-2/凋亡信号调节激酶1信号通路在曲格列酮诱导的人肝细胞损伤中起关键作用。
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Troglitazone-induced hepatic mitochondrial proteome expression dynamics in heterozygous Sod2(+/-) mice: two-stage oxidative injury.曲格列酮诱导杂合子Sod2(+/-)小鼠肝脏线粒体蛋白质组表达动态变化：两阶段氧化损伤
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Integrative toxicoproteomics implicates impaired mitochondrial glutathione import as an off-target effect of troglitazone.整合毒理学蛋白质组学表明，谷胱甘肽导入受损是曲格列酮的一种非靶标效应。
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Increased susceptibility to troglitazone-induced mitochondrial permeability transition in type 2 diabetes mellitus model rat.2型糖尿病模型大鼠对曲格列酮诱导的线粒体通透性转换的易感性增加。
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Mechanisms of troglitazone hepatotoxicity.曲格列酮肝毒性的机制。
Chem Res Toxicol. 2003 Jun;16(6):679-87. doi: 10.1021/tx034033e.
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Mitochondrial permeability transition as a potential determinant of hepatotoxicity of antidiabetic thiazolidinediones.线粒体通透性转换作为抗糖尿病噻唑烷二酮类药物肝毒性的潜在决定因素。
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Usefulness of in vitro combination assays of mitochondrial dysfunction and apoptosis for the estimation of potential risk of idiosyncratic drug induced liver injury.线粒体功能障碍与细胞凋亡的体外联合检测在评估特异质性药物性肝损伤潜在风险中的应用价值
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Agree that idiosyncratic hepatotoxicity in TRO-treated patients is uncertain, but concerned about the data.同意托法替布（TRO）治疗患者的特异质性肝毒性尚不确定，但对相关数据感到担忧。
Toxicol Sci. 2003 Feb;71(2):282; author reply 282-4. doi: 10.1093/toxsci/71.2.282.

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