Itgam, also known as Integrin Subunit α M, encodes the CD11b chain of the Mac-1 integrin. Mac-1 integrin is involved in cell adhesion, phagocytosis, and regulation of inflammatory cytokine production in macrophages. It plays a crucial role in the immune response and inflammation-related pathways [6].

In ischemic stroke, Itgam was identified as a critical gene. Its overexpression was found in patients, and its modulation influenced the secretion of inflammatory cytokines like IL-1β, IL-6, and TNF-α, and affected neuronal apoptosis, suggesting it may be a potential therapeutic target [1].

In systemic lupus erythematosus (SLE), multiple meta-analyses have shown a significant association between Itgam gene polymorphism (such as rs1143679) and SLE susceptibility in different ethnic populations. The A allele of rs1143679 was more prevalent in SLE patients [2,5,7].

In neutrophilic asthma, Itgam was identified as a key target to distinguish the disease from healthy/non-NA individuals, with a strong correlation between Itgam and macrophages [3].

In diabetic nephropathy and atherosclerosis, Itgam was found to be a key gene involved in basement membrane alterations, mainly expressed in macrophages, and may contribute to basement membrane lesions [4].

In Kawasaki disease, NFIL3 was found to aggravate human coronary artery endothelial cell injury by promoting Itgam transcription [8].

In conclusion, Itgam is essential in immune-related functions and inflammation-associated pathways. Its dysregulation is implicated in multiple diseases including ischemic stroke, SLE, neutrophilic asthma, diabetic nephropathy, atherosclerosis, and Kawasaki disease. Studies on Itgam, especially through gene-based models in vivo, have provided insights into the disease mechanisms, highlighting its potential as a therapeutic target in these disease areas.