Renal ischemia-reperfusion injury (IRI) remains a major challenge impacting graft survival following transplantation. During the ischemic phase, mitochondrial dysfunction leads to adenosine triphosphate (ATP) depletion and calcium overload. Upon reperfusion, reactive oxygen species (ROS) are generated, exacerbating mitochondrial damage and triggering inflammatory responses. This process is associated not only with delayed graft function (DGF) but also with allograft dysfunction. Mitochondria, serving as the high-energy-demand hub of the kidney, require precise regulation of their dynamic balance and mitophagy. Mitophagy selectively removes damaged mitochondria to maintain cellular homeostasis. In the context of IRI, mitophagy exhibits a bidirectional regulatory role: moderate activation can improve energy metabolism, whereas excessive or insufficient activation may exacerbate renal injury. To provide new insights for enhancing graft survival rates, this paper examines the molecular mechanisms, therapeutic targets, and dual regulatory roles involved.