Our key results demonstrated that in ALI-afflicted mice, AMSCs exhibited targeted pulmonary tropism, homing in on injured alveolar regions, where they restored the morphology and functionality of damaged tissues and organelles, re-established lung barrier function, and attenuated the aberrantly activated TLR4/NF-κB/MAPK and TGF-β/Smad pathways associated with inflammation. Here, NFKB1 is linked to acute respiratory distress syndrome.