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Abstract Chronic respiratory diseases (CRDs), including pulmonary fibrosis (PF), chronic obstructive pulmonary disease (COPD), asthma, and lung cancer, are sustained by recurrent epithelial injury, oxidative stress, inflammation, and defective tissue repair. DNA damage and dysregulated autophagy are common pathophysiological features of CRDs, but their mechanistic crosstalk has not been integrated across disease contexts.
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