Abstract
Introduction: Amiodarone (AD) is a well known anti arrhythmic drug, but is limited by its potential side effects. Severe pulmonary toxicity is reported in patients receiving amiodarone, with the most common histological finding being chronic interstitial pneumonia. Apoptosis of alveolar epithelial cells type II (AECII) was reported in a rat model of amiodarone induced pulmonary toxicity. However, the underlying molecular mechanisms remain unknown. We aimed to establish a mouse model for AD induced pulmonary fibrosis and study the involved molecular mechanisms.
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