IL-1β inhibition may alleviate aortic aneurysm immunopathology, review suggests

In recent years, the incidence of aortic aneurysms has been on the rise due to population aging, increased burden of chronic diseases, lifestyle changes, and advances in clinical technology. Identifying therapeutic targets for aortic aneurysms has become paramount in alleviating their immunopathology. Key pathological factors in aneurysm formation include inflammatory cell infiltration, metalloproteinase-mediated degradation of elastin and collagen, and increased proinflammatory factor activity. Macrophages play a pivotal role in vascular inflammation. Their polarization toward the M1 phenotype promotes IL-1β production. IL-1β contributes to aortic aneurysm inflammation by recruiting immune cells to the vascular wall, enhancing matrix metalloproteinase activation, and inducing apoptosis and phenotypic transformation of vascular smooth muscle cells. Thoracic and abdominal aortic aneurysms differ in terms of etiology, the cellular origin of IL-1β, and their degree of inflammation dependence, suggesting that IL-1β-related mechanisms are disease-specific. Current research indicates that inhibiting IL-1β activity and expression can alleviate aortic aneurysms. This review discusses the mechanisms by which IL-1β promotes aortic aneurysm inflammation and the principles underlying the alleviation of aortic aneurysm immunopathology.