Protection against cigarette smoke-induced chronic obstructive pulmonary disease via activation of the SIRT1/FoxO1 axis by targeting microRNA-132

Inhibition of miR-132 may serve as a therapeutic strategy for CS-induced COPD.

COPD was induced in C57BL/6J male mice by exposing them to cigarette smoke (CS) for 8 weeks. A miR-132 knockout mouse model was used to assess the role of miR-132 in CS-induced COPD. Lung tissue apoptosis was evaluated using TUNEL assays and histopathology, along with lung functional tests which were performed to assess CS-induced lung injury.

To investigate the biological role of miR-132 in a murine model of chronic obstructive pulmonary disease (COPD) via activation of the SIRT1/FoxO1 axis.

Elevated miR-132 expression was observed in lung tissues and bronchoalveolar lavage fluid in COPD mice. miR-132 depletion improved lung function, restored lung tissue morphology, and reduced apoptosis. Target prediction software identified miR-132 as a potential repressor of SIRT1. In COPD mice, SIRT1 and FoxO1 expression were reduced, but miR-132 knockout restored their levels.