Abstract
Hyperoxia-induced acute lung injury (HALI) is a severe side effect of refractory hypoxemia treatment, for which no effective therapeutic strategy is available. Here, we found that the lung miR-21-5p level was significantly decreased in the rats subjected to hyperoxia. Further, we presented evidence that miR-21-5p was a crucial regulator of mitophagy and mitochondrial dysfunction. Moreover, it proved that miR-21-5p regulated hyperoxia-induced mitophagy and mitochondrial dysfunction by directly binding to the target gene PGAM5. In conclusion, for the first time, we found that miR-21-5p could directly suppress mitophagy and mitochondrial damage during HALI formation.