Ischemia-reperfusion injury (IRI) is one of the key factors leading to organ dysfunction and transplant failure. Its mechanism is complex and not yet fully elucidated, with limited treatment options. During IRI, various forms of cell death are activated, including apoptosis, pyroptosis, autophagy, and programmed necrosis. Ferroptosis, a novel form of programmed cell death characterized by iron-dependent reactive oxygen species (ROS) and lipid peroxidation accumulation, has been shown to play a significant role in IRI. By regulating iron, glucose, amino acid, and lipid metabolism, as well as signaling pathways, ferroptosis exacerbates organ IRI. Inhibiting ferroptosis has been proven to reduce IRI damage in multiple organs effectively, but compared to other forms of programmed cell death, the mechanisms of ferroptosis in IRI are still less studied. IRI is closely related to ROS production, which induces lipid peroxidation reactions and damages cell membrane structures, thereby being tightly linked to ferroptosis. This paper discusses the multifaceted roles of ferroptosis in organ IRI by examining the regulatory pathways of iron metabolism, lipid peroxidation, antioxidant systems, and other factors involved in cellular ferroptosis, aiming to provide references for IRI-related experiments and clinical treatments.