
The cause of bronchopulmonary dysplasia (BPD) is not fully understood, but recent studies suggest that impaired autophagy due to insufficient activation of AMP-activated protein kinase (AMPK) may play a role. In a murine model of BPD induced by neonatal hyperoxia exposure, impaired autophagy was associated with increased inflammation in alveolar macrophages (AMs) and worsened disease severity. Treatment with the AMPK activator AICAR resulted in increased AMPK activation and autophagic activity, which protected against hyperoxia-induced lung damage by decreasing proinflammatory signaling in AMs via autophagy-dependent mechanisms.
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