miR-146a plays a critical role in limiting the inflammatory response to ischemia-reperfusion. After IRI, the induction of TLR/IL-1R signaling leads to the activation of the NF-κB pathway, promoting CXCL8 secretion by tubular cells. This process facilitates immune cell recruitment, leading to tubular injury and interstitial fibrosis. NF-κB activation also induces miR-146a expression, which indirectly suppresses CXCL8 secretion by targeting IRAK1, thus balancing the inflammatory consequences of renal IRI.