Iron is an essential trace element for the human body and is critical for vital cellular processes, such as DNA synthesis, respiration, and oxygen transport. The body maintains iron homeostasis through a coordinated balance of absorption, utilization, storage, and distribution. Both iron deficiency and excess can lead to pathologies, with the latter triggering lipid peroxidation and DNA mutations via the Fenton reaction, potentially causing ironinduced cell death in severe cases. Although iron overload can inflict severe damage on multiple organs, including the brain, liver, spleen, heart, ovaries, and kidneys, the mechanisms that regulate iron homeostasis in response to overload are not fully understood. Various animal models have been developed to help elucidate these mechanisms, each reflecting different aspects of iron overload relevant to human diseases, and selection of the most appropriate animal model is needed for the accurate simulation of the pathological and physiological states associated with human iron overload-related diseases. This review synthesizes recent literature on animal models pertinent to iron overload, to offer insights to support the development and analysis of models for diseases related to iron overload.