Ferroptosis is a newly discovered form of regulated cell death. Ferroptosis is an iron-dependent lipid peroxidation reaction of cell membrane lipids, and it is closely related to the occurrence and development of many inflammatory diseases, such as ischemia-reperfusion injury, nonalcoholic steatohepatitis, and tumors. Although the precise role of ferroptosis in these inflammatory diseases is still unclear, recent evidence indicates that the association between ferroptosis and inflammatory diseases is related to the interaction of ferroptosis and inflammatory microenvironments. In inflammatory microenvironments, ferroptosis can be regulated by metabolic changes or the secretion of related substances between microorganisms and host cells or between host cells. At the same time, ferroptotic cells can also recruit immune cells by releasing injury-related molecular patterns, which in turn induces the generation of inflammatory microenvironments. Molecular crosstalk between ferroptosis and other cell death types also exists in inflammatory microenvironments. In addition, the interaction of ferroptosis and the tumor microenvironment is also correlated with tumor growth. This article reviews the main metabolic processes of ferroptosis, describes the interaction mechanism between ferroptosis and inflammatory microenvironments, and summarizes the role of ferroptosis in the treatment of diseases.