Fig. 9

Schematic of CIE-induced P2 × 7R signaling promoting neuroinflammation. We summarize from this study that CIE leads to P2 × 7R activation, resulting in increased levels of extracellular ATP, EV-ATP, and a higher number of EVs. The released eATP further activates P2 × 7R through paracrine signaling, amplifying the response. The EVs also contain elevated mtDNA copy numbers, which may serve as DAMPs, contributing to inflammation in brain endothelial cells. P2 × 7R inactivation significantly reduces CIE induced responses, suggesting a novel mechanism of brain injury during CIE exposure via P2 × 7R signaling”. Figure created using Biorender.com