CCL2 and acute kidney injury: In vitro and vivo studies showed that IS accumulats in renal tissue after I/R AKI and induces free radical [27], ROS production, and release of many cytokines and chemokines, such as monocyte chemotactic protein-1 and EGF receptor, leading to impairment of proximal tubular and endothelial cell function through ERK and JNK pathways [38–40].