Inflammatory bowel disease (IBD), encompassing two subtypes, ulcerative colitis, and Crohn's disease, is a chronic, non-specific gastrointestinal disorder with a complex etiology stemming from various factors. The incidence of IBD has been steadily rising in the past few years, causing great physical and mental strain on patients. Traditional IBD therapeutic drugs include anti-inflammatory drugs, immunosuppressants, and biologics; however, they may have serious adverse effects. This has fueled active clinical research exploring new targets for IBD treatment, focusing on the unique metabolic pathways and functions of macrophages. Macrophage immune metabolism plays a crucial role in IBD; however, the mechanism is unclear. This review discussed the role and potential mechanisms of macrophage metabolic reprogramming in IBD and the link between macrophages and ferroptosis. While these findings from preclinical models suggest novel therapeutic avenues for IBD, such as targeting macrophage metabolic reprogramming and hypothetical approaches like ferroptosis modulation, their clinical applicability remains speculative; rigorous disease-specific validation is imperative.
Zhang et al. (Fri,) studied this question.