mTOR and autophagy in acute lung injury pathogenesis and therapeutic potential

Acute lung injury (ALI) poses a significant clinical challenge due to its high morbidity and mortality rates. Current treatment options are limited in their efficacy, necessitating the exploration of novel therapeutic targets. The mammalian target of rapamycin (mTOR), a crucial regulator of various cellular processes, has been implicated in the pathogenesis of ALI. Autophagy, a tightly regulated cellular degradation process controlled by mTOR, plays a pivotal role in the pathogenesis of ALI and cellular homeostasis. Mounting evidence also suggests that the mTOR pathway and autophagy play crucial roles in the pathogenesis and regulation of ALI. Herein, we reviewed the current understanding of how mTOR signaling and autophagy intersect in the context of ALI, with a focus on their roles across different cell types. This analysis highlights their dual roles in either promoting pulmonary injury or providing protection, depending on the specific cell types and different ALI models. Insights into the intricate balance between mTOR-mediated pathways and autophagic responses provide a foundation for developing targeted therapeutic strategies aimed at alleviating ALI through the modulation of these pathways. This review underscores the therapeutic potential of targeting mTOR and autophagy, presenting innovative and promising approaches for improving the clinical management and outcomes of ALI.