Hepatotoxicity: From Pathology to Novel Therapeutic Approaches (2nd Edition)
A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".
Deadline for manuscript submissions: 31 July 2025 | Viewed by 246
Special Issue Editor
Interests: signal transduction in drug-induced hepatotoxicity; regulation of mitochondrial bioenergetic signaling in hepatotoxicity; metabolic dysfunction-associated steatotic liver disease (MASLD); alcoholic hepatitis; identification of therapeutic targets; cellular mechanisms of hepatotoxicity
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Special Issue Information
Dear Colleagues,
Hepatotoxicity can be caused by drug medications, chemical agents, dietary supplements, solvents, and chronic alcohol drinking. As the main organ that metabolizes and detoxifies chemicals, the liver is susceptible to the toxicity of these agents, leading to acute and chronic liver disease. Most drug-induced liver injuries (DILIs) improve after drug withdrawal, and are dose-dependent; this form of liver injury is called predictable hepatotoxicity. In other cases, liver injury is caused by unpredictable (idiosyncratic) hepatotoxicity in susceptible individuals. Active signal transduction pathways and mitochondrial dysfunction are important in determining cell survival or death. Understanding the mechanisms and signal regulation in hepatotoxicity can aid in the production of therapeutic target molecules for safe and effective treatment.
This Special Issue on hepatotoxicity aims to collect and disseminate recent findings on the mechanisms, pathophysiology, and signal transduction pathways in hepatotoxicity and advancements in therapy. Original articles, communications, and review articles are welcome.
Dr. Sanda Win
Guest Editor
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Keywords
- cell death
- reactive metabolites
- oxidative stress
- stress signaling
- mitochondria
- adaptive immunity
- HLA associations
- hepatotoxicity
- drugs
- liver injury
- adverse drug reaction
- drug-induced autoimmune hepatitis
- idiosyncratic-drug-induced liver injury
- bile acid
- drug-induced cholestasis
- hepatotoxins
- steatosis
- fibrosis
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