ArticleThe journal of pathology. Clinical research2015
Regulation of macroautophagy in amiodarone-induced pulmonary fibrosis.
Article in The journal of pathology. Clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Deficient chaperone-mediated autophagy drives multiorgan fibrogenesis via SMAD2/4 stabilization to sustain TGFβ-SMAD signaling.Acta pharmacologica Sinica · 2026Article
- Network toxicology reveals key genes of amiodarone induced pulmonary fibrosis: based on machine learning and SHAP analysis.Frontiers in pharmacology · 2026Article
- Nanoscale Imaging of Biological Tissues: Techniques, Challenges and Emerging Frontiers.Nanomaterials (Basel, Switzerland) · 2025Review
- Amiodarone promoted autophagy and enhanced tissue repair, outperforming albendazole in treating the muscular phase of experimental trichinellosis spiralis.Journal of molecular histology · 2025Article
- Amiodarone Therapy: Updated Practical Insights.Journal of clinical medicine · 2024Review
- Variable radiographic and histologic presentations of amiodarone-related interstitial lung disease and the importance of avoiding re-exposure.Respirology case reports · 2023Article
- Animal models of drug-induced pulmonary fibrosis: an overview of molecular mechanisms and characteristics.Cell biology and toxicology · 2022Review
- Therapeutic induction of Bcl2-associated athanogene 3-mediated autophagy in idiopathic pulmonary fibrosis.Clinical and translational medicine · 2022Article
- Caveolin-1 scaffolding domain peptide abrogates autophagy dysregulation in pulmonary fibrosis.Scientific reports · 2022Article
- Amiodarone induced lung disease.Archive of clinical cases · 2022Article
- TGFβ promotes fibrosis by MYST1-dependent epigenetic regulation of autophagy.Nature communications · 2021Observational
- Volume electron microscopy: analyzing the lung.Histochemistry and cell biology · 2021Review
- Article
- Susceptibility of microtubuleFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Is Progression of Pulmonary Fibrosis due to Ventilation-induced Lung Injury?American journal of respiratory and critical care medicine · 2019Review
- Thyroid hormone: a resurgent treatment for an emergent concern.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Amiodarone promotes cancer cell death through elevated truncated SRSF3 and downregulation of miR-224.Oncotarget · 2018Article
- Toxicity of orally inhaled drug formulations at the alveolar barrier: parameters for initial biological screening.Drug delivery · 2017Article
- Influences of innate immunity, autophagy, and fibroblast activation in the pathogenesis of lung fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2016Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amiodarone (AD) is an iodinated benzofuran derivative, especially known for its antiarrhythmic properties. It exerts serious side-effects even in patients receiving low doses. AD is well-known to induce apoptosis of type II alveolar epithelial cells (AECII), a mechanism that has been suggested to play an important role in AD-induced lung fibrosis. The precise molecular mechanisms underlying this disease are, however, still unclear. Because of its amphiphilic nature, AD becomes enriched in the lysosomal compartments, affecting the general functions of these organelles. Hence, in this study, we aimed to assess the role of autophagy, a lysosome-dependent homeostasis mechanism, in driving AECII apoptosis in response to AD. In vitro, AD-treated MLE12 and primary AECII cells showed increased proSP-C and LC3B positive vacuolar structures and underwent LC3B-dependent apoptosis. In addition, AD-induced autophagosome-lysosome fusion and increased autophagy flux were observed. In vivo, in C57BL/6 mice, LC3B was localised at the limiting membrane of lamellar bodies, which were closely connected to the autophagosomal structures in AECIIs. Our data suggest that AD causes activation of macroautophagy in AECIIs and extensive autophagy-dependent apoptosis of alveolar epithelial cells. Targeting the autophagy pathway may therefore represent an attractive treatment modality in AD-induced lung fibrosis.
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Registered trials
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.