C3AR1 and acute kidney injury: Furthermore, C3aR-deficient (C3aR-/-) mice were generated to knockdown the C3a receptor, and it was demonstrated that the C3a-C3aR axis further contributes to IRI-AKI through the ERK/ROS/PAD4/NETosis pathway (93), highlighting C3a-C3aR1 as a highly promising therapeutic target for future NETosis-directed therapies.