Drug-Induced Hepatotoxicity: From Pathology to Novel Therapeutic Approaches

Dear Colleagues,

Drug-induced liver injury (DILI) is a cause of acute and chronic liver disease. DILI is caused specifically by medications (drugs/herbal), chemical agents, and dietary supplements, and most DILIs improve after drug withdrawal.

The liver is the main organ for metabolized and detoxification chemicals and is susceptible to the toxicity of these agents. Drugs associated with DILIs may cause injury in a dose-dependent, predictable hepatotoxicity (e.g., acetaminophen) or in an unpredictable (idiosyncratic) hepatotoxicity in susceptible individuals. Most idiosyncratic drug reactions are caused by immune-mediated toxicity. Idiosyncratic DILI is mainly mediated by the innate or adaptive immune response, involving death ligands such as TNFα and FasL. TNF-α and FasL bind to death receptors of hepatocytes, triggering apoptotic cell death.

Drugs or their toxic metabolites cause the activation of MAP kinases or deactivation of signaling pathways. Then, it causes the impairment of mitochondrial function, oxidative stress, mitochondria damaged, and hepatocyte death.

Moreover, the endogenous defense system of the liver is made up of endogenous nonprotein antioxidants and endogenous protein antioxidants. The main endogenous antioxidants are glutathione, lipoic acid, bilirubin, ferritin, superoxide dismutase, catalase, and glutathione peroxidase. Their main function is to maintain redox homeostasis in the liver.

The aim of this Special Issue on Drug-Induced Hepatotoxicity is to discuss updated recent findings in mechanisms of drug induced hepatoxicity and potential therapeutic targets. Original articles and review articles on the following topics are welcome.

Dr. Sanda Win
Guest Editor

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