摘要

Neutrophil extracellular traps, originally discovered as a mechanism to combat microbial infection, have recently been implicated in tissue damage including acute kidney injury. Raup-Konsavage et al. now present further insights to demonstrate a critical role of neutrophil peptidyl arginine deiminase-4 in the formation of neutrophil extracellular trap, inflammation, and tissue damage in ischemic acute kidney infection. Targeting peptidyl arginine deiminase-4 and/or neutrophil extracellular trap may offer a new therapeutic strategy for acute kidney infection.