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| http://dx.doi.org/10.1164/rccm.201608-1635ED | DOI Listing |
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Artemisinin protected human bronchial epithelial cells from amiodarone-induced oxidative damage via 5'-AMP-activated protein kinase (AMPK) activation.
Redox Rep
December 2025
Pharmaceutical Science, Faculty of Health Sciences, University of Macau, Taipa, People's Republic of China.
Background: Amiodarone, a common antiarrhythmic drug, is known for its severe side effects, including pulmonary toxicity, which involves oxidative stress and apoptosis. Artemisinin, an antimalarial drug, has shown cytoprotective properties by inhibiting oxidative stress and apoptosis. This study investigated the protective effects of artemisinin against amiodarone-induced toxicity in human bronchial epithelial cells (BEAS-2B) and mouse models.
View Article and Find Full Text PDFNRP1 overexpression potentially enhances osimertinib resistance in NSCLC via activation of the PI3K/AKT signaling pathway.
Am J Cancer Res
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Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Soochow University Suzhou 215006, Jiangsu, China.
Resistance to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is the main cause of mortality in lung cancer. This study aimed to investigate the roles of neuropilin 1 (NRP1) in non-small cell lung cancer (NSCLC). NRP1 expression was assessed in tumor tissues from patients with osimertinib-resistant (OR) NSCLC and osimertinib-responsive NSCLC as well as in patients with paracancerous NSCLC tissues who did not undergo radiotherapy or chemotherapy.
View Article and Find Full Text PDFRisk factors for mediastinal lymph node metastases in early-stage non-small-cell lung cancer and prediction model establishment.
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Department of Orthopaedic Surgery, The Second Affiliated Hospital of Guangzhou Medical University Guangzhou 510260, Guangdong, China.
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View Article and Find Full Text PDFThirty-day unplanned readmissions following hospitalization for atrial fibrillation in a tertiary Syrian center: A real-world observational cohort study.
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Department of Cardiovascular Sciences, University of Leicester, Leicester, United Kingdom.
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Cancer cells within tumors exhibit a wide range of phenotypic states driven by non-genetic mechanisms in addition to extensively studied genetic alterations. Conversions among cancer cell states can result in intratumoral heterogeneity which contributes to metastasis and development of drug resistance. However, mechanisms underlying the initiation and/or maintenance of such phenotypic plasticity are poorly understood.
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