STING hinders XIAP-mediated degradation of NLRP3 to lock the inflammasome in a hyperactivated state during pulmonary ischemia-reperfusion injury.
Pulmonary ischemia-reperfusion (I/R) injury activates the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome to drive sterile inflammation. Although stimulator of interferon genes (STING) signaling primes NLRP3 transcription, its post-translational control over NLRP3 stability during lung I/R remai...