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Boosting ALDH1A1 reverses PM2.5-induced airway dysfunction, study finds

A University of Osaka-led team traced airway injury to reactive aldehyde buildup, pinpointing ALDH1A1 augmentation as a means to revive the lungs’ self-cleaning function

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Scientists have identified how air pollution damages lung function – and potentially how to treat it
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Overview

  • PM2.5 particles such as dust, vehicle exhaust and wildfire smoke penetrate deeply into the respiratory tract and rank as the second leading global mortality risk
  • Oxidative injury from PM2.5 exposure produces lipid peroxide-derived aldehydes that damage airway cilia and impair mucociliary clearance
  • Mice lacking the ALDH1A1 enzyme showed reduced cilia formation and heightened susceptibility to respiratory infections after pollutant exposure
  • Pharmacological enhancement of ALDH1A1 levels in mice restored mucociliary function despite ongoing exposure to PM2.5
  • Published June 3 in the Journal of Clinical Investigation, the multi-institutional study led by The University of Osaka suggests ALDH1A1 as a promising therapeutic target for pollution-related lung diseases