Autophagy
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Autophagy, a cellular program for organelle and protein turnover, represents primarily a cell survival mechanism. However, the role of autophagy in the regulation of apoptosis remains unclear. We have observed increases in morphological and biochemical indicators of autophagy in human lung from patients with chronic obstructive pulmonary disease (COPD). ⋯ Caveolin-1 knockout mice exhibit increased autophagic markers, apoptosis, and airspace enlargement in the lung in response to chronic cigarette smoke. These studies demonstrate that LC3B can promote tissue injury during chronic cigarette smoke exposure, and suggest a mechanism by which LC3B, through interactions with caveolin-1 and Fas, can regulate apoptosis. Targeting the autophagic pathway may represent an experimental therapeutic strategy when designing new approaches to COPD treatment.