Previous studies have demonstrated the crucial role of mitochondria in kidney energy metabolism and that mitochondrial dysfunction is a key factor in the pathogenesis of AKI.[35, 36, 37] Additionally, exogenous irisin had been demonstrated to target mitochondria when cells were under stress condition.[38] Therefore, we investigated whether MCM@MOF@irisin has enhanced mitochondrial targeting capability that could further benefit its therapeutic effect. Here, FNDC5 is linked to acute kidney injury.