Crosstalk between ferroptosis and macrophages: potential value for targeted treatment in diseases.

Abstract

Ferroptosis is a newly identified form of programmed cell death that is connected to iron-dependent lipid peroxidization. It involves a variety of physiological processes involving iron metabolism, lipid metabolism, oxidative stress, and biosynthesis of nicotinamide adenine dinucleotide phosphate, glutathione, and coenzyme Q10. So far, it has been discovered to contribute to the pathological process of many diseases, such as myocardial infarction, acute kidney injury, atherosclerosis, and so on. Macrophages are innate immune system cells that regulate metabolism, phagocytize pathogens and dead cells, mediate inflammatory reactions, promote tissue repair, etc. Emerging evidence shows strong associations between macrophages and ferroptosis, which can provide us with a deeper comprehension of the pathological process of diseases and new targets for the treatments. In this review, we summarized the crosstalk between macrophages and ferroptosis and anatomized the application of this association in disease treatments, both non-neoplastic and neoplastic diseases. In addition, we have also addressed problems that remain to be investigated, in the hope of inspiring novel therapeutic strategies for diseases.