Ferroptosis, an iron-dependent form of programmed cell death, plays a critical role in various diseases, including liver disease, neurological disorders, lung injury, heart injury, cancer, and others. Exosomes, which are extracellular vesicles, have emerged as promising therapeutic agents due to their low immunogenicity, low toxicity, and ability to penetrate biological barriers. They can modulate ferroptosis by regulating key pathways such as the system Xc-/GSH/GPX4 axis, the NAD(P)H/FSP1/CoQ10 axis, iron metabolism, and lipid metabolism. Exosome-regulated ferroptosis can act as a double-edged sword, either promoting or inhibiting disease progression depending on the context. This review summarizes the mechanisms by which exosomes from different sources regulate ferroptosis in various diseases and their potential applications in treatment. Exosomes can influence ferroptosis through multiple pathways, including the regulation of iron metabolism, lipid metabolism, and the expression of key proteins such as SLC7A11, GPX4, FSP1, and Nrf2. The review also discusses the role of exosome-regulated ferroptosis in tissue repair and its potential as a therapeutic strategy for various diseases. Additionally, the review highlights the importance of understanding the interactions between exosomes, ferroptosis, and other biological processes such as inflammation and immunity, which may lead to more effective therapeutic approaches. The study emphasizes the need for further research to fully understand the mechanisms of exosome-regulated ferroptosis and its potential applications in clinical settings.Ferroptosis, an iron-dependent form of programmed cell death, plays a critical role in various diseases, including liver disease, neurological disorders, lung injury, heart injury, cancer, and others. Exosomes, which are extracellular vesicles, have emerged as promising therapeutic agents due to their low immunogenicity, low toxicity, and ability to penetrate biological barriers. They can modulate ferroptosis by regulating key pathways such as the system Xc-/GSH/GPX4 axis, the NAD(P)H/FSP1/CoQ10 axis, iron metabolism, and lipid metabolism. Exosome-regulated ferroptosis can act as a double-edged sword, either promoting or inhibiting disease progression depending on the context. This review summarizes the mechanisms by which exosomes from different sources regulate ferroptosis in various diseases and their potential applications in treatment. Exosomes can influence ferroptosis through multiple pathways, including the regulation of iron metabolism, lipid metabolism, and the expression of key proteins such as SLC7A11, GPX4, FSP1, and Nrf2. The review also discusses the role of exosome-regulated ferroptosis in tissue repair and its potential as a therapeutic strategy for various diseases. Additionally, the review highlights the importance of understanding the interactions between exosomes, ferroptosis, and other biological processes such as inflammation and immunity, which may lead to more effective therapeutic approaches. The study emphasizes the need for further research to fully understand the mechanisms of exosome-regulated ferroptosis and its potential applications in clinical settings.