Figure 10.

EV-mediated lung–brain axis. The AMs in early injured lungs release EVs that contain an increased cargo of ASC. These EVs contribute to bronchopulmonary dysplasia pathogenesis by inducing lung inflammation and inhibiting alveolarization and vascularization. These EVs can be released to the circulation, cross the BBB and be taken up by neural cells, and the ASC cargo can activate GSDMD in specific neural cells and result in brain injury by activating microglia and inducing cell death, possibly through apoptosis, pyroptosis, and necroptosis mechanisms. The molecular and cellular changes can lead to long-term NDI. BBB = blood–brain barrier; NDI = neurodevelopmental impairment.