Ischemia-Reperfusion Injury (IRI) in kidney Transplantation (KTx) is intricately associated with acute rejection, Delayed Graft   Function (DGF), and allograft failure. Substantial evidence underscores a significant correlation between mitochondrial dysfunction   and the pathophysiology of IRI. Mitochondria serve as essential regulators of cellular energy metabolism, redox homeostasis,   and apoptosis, thereby contributing to IRI through a myriad of mechanisms. This review summarizes the pathological role of   mitochondria in renal IRI and critically evaluates recent advancements in mitochondria-targeted therapies designed to ameliorate   transplant-related IRI.