ArticleArchives of toxicology2020
Autophagy alleviates amiodarone-induced hepatotoxicity.
Article in Archives of toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- A Lipid-Conjugation Strategy for Intracellular Reactive Oxygen Species Control in Hepatic Cells.Angewandte Chemie (International ed. in English) · 2026Article
- Hepatic cellular stress response pathways exhibit species differences in basal and inducible activity.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Smoldering Amiodarone-Induced Decompensated Cirrhosis: Cumulative Dose-Related Toxicity.Case reports in gastrointestinal medicine · 2026Article
- Integration of cAMP and TRPV4 Signaling to Optimize Collagen Remodeling for Management of Fibrosis.Cells · 2025Review
- Betaine Mitigates Paclitaxel-Induced Hepatotoxicity in Rats by Regulating Oxidative Stress, Inflammation, Apoptosis, and Autophagy.Food science & nutrition · 2025Article
- Changes in Hepatic Density Due to Oral Amiodarone-induced Liver injury Shown by Computed Tomography.Internal medicine (Tokyo, Japan) · 2025Article
- Human induced pluripotent stem cells-derived liver organoids grown on a Biomimesys® hyaluronic acid-based hydroscaffold as a new model for studying human lipoprotein metabolism.Bioengineering & translational medicine · 2024Article
- Amiodarone-Induced Liver Attenuation on CT Scan: Alarming Signal for Toxicity and Prompt Discontinuation.Cureus · 2023Article
- Article
- Protective Role of Amiodarone on Reperfusion Arrhythmia in Patients of Acute Myocardial Infarction with Percutaneous Coronary Intervention Treatment.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Cell Models and Omics Techniques for the Study of Nonalcoholic Fatty Liver Disease: Focusing on Stem Cell-Derived Cell Models.Antioxidants (Basel, Switzerland) · 2021Review
- BH3-only protein expression determines hepatocellular carcinoma response to sorafenib-based treatment.Cell death & disease · 2021Article
- New Avenues for Treatment and Prevention of Drug-Induced Steatosis and Steatohepatitis: Much More Than Antioxidants.Advances in therapy · 2021Review
- Role of autophagy in drug induced liver injury.Archives of toxicology · 2020Article
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amiodarone is a widely used antiarrhythmic drug that can cause the development of steatohepatitis as well as liver fibrosis and cirrhosis. The molecular mechanisms of amiodarone-mediated liver injury remain largely unknown. We therefore analyzed amiodarone-mediated hepatocellular injury in patients with chronic heart failure, in primary hepatocytes and HepG2 cells. We found that amiodarone-treated patients with chronic heart failure revealed significantly higher serum levels of caspase-cleaved keratin-18, an apoptosis biomarker, compared to healthy individuals or patients not receiving amiodarone. Furthermore, amiodarone treatment of hepatocytes resulted in apoptosis associated with lipid accumulation and ER-stress induction. Liver cell steatosis was accompanied by enhanced de novo lipogenesis which, after reaching peak levels, declined together with decreased activation of ER stress. The decline of amiodarone-mediated lipotoxicity was associated with protective autophagy induction. In contrast, in hepatocytes treated with the autophagy inhibitor chloroquine as well as in autophagy gene (ATG5 or ATG7)-deficient hepatocytes, amiodarone-triggered toxicity was increased. In conclusion, we demonstrate that amiodarone induces lipid accumulation associated with ER stress and apoptosis in hepatocytes, which is mirrored by increased keratin-18 fragment serum levels in amiodarone-treated patients. Autophagy reduces amiodarone-mediated lipotoxicity and could provide a therapeutic strategy for protection from drug-induced liver injury.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.