Iron is an essential trace element for the human body, critical for vital cellular processes such as DNA synthesis, respiration, and oxygen transport. The body meticulously maintains iron homeostasis through a coordinated balance of absorption, utilization, storage, and distribution. Both iron deficiency and excess can lead to pathologies; the latter can trigger lipid peroxidation and DNA mutations through the Fenton reaction, potentially causing iron-induced cell death in severe cases. Iron overload is recognized to inflict significant damage on multiple organs, including the brain, liver, spleen, heart, ovaries, and kidneys. Despite this, the mechanisms that regulate iron homeostasis in response to overload are not fully understood.To elucidate these mechanisms, various animal models have been developed, each reflecting different aspects of iron overload (IOL) relevant to human diseases. Accurately simulating the pathological and physiological states associated with human IOL-related diseases necessitates the selection of the most appropriate animal models. This review synthesizes recent literature on animal models pertinent to iron overload, aiming to offer insights for the development and analysis of models for diseases related to iron overload.