Abstract
Iron overload is a pathological condition characterized by the abnormal accumulation of iron within the body, which may result from excessive iron intake, disorders of iron metabolism, or specific disease states. This condition can lead to significant health complications and may pose life-threatening risks. The excessive accumulation of iron can induce cellular stress, adversely affecting the structure and function of mitochondria, thereby compromising overall organ function. Given the critical role of mitochondria in cellular metabolism and homeostasis, it is imperative to investigate how mitochondrial dysfunction induced by iron overload contributes to disease progression, as well as to explore mitochondrial-related pathways as potential therapeutic targets for various iron overload disorders. This review examines the mechanisms by which mitochondria are implicated in iron overload-induced damage, including increased oxidative stress, mitochondrial DNA damage, and disruptions in energy metabolism. Additionally, it addresses the relationship between these processes and various forms of programmed cell death, as well as alterations in mitochondrial dynamics. Furthermore, the review discusses strategies aimed at alleviating and mitigating the complications associated with iron overload in patients by targeting mitochondrial pathways.