Thromboangiitis obliterans(TAO)is an inflammatory vascular disease that primarily affects small and medium-sized blood vessels in the extremities,and endothelial cell activation plays a key role in the development of the disease.Various physiopathological processes such as immune complex deposition,high levels of inflammatory immune cells and inflammatory cytokines,overexpression of inducible nitric oxide synthase(iNOS),oxidative stress,endoplasmic reticulum stress,mitochondrial dysfunction,copper homeostasis,iron metabolism,and glycolysis all promote endothelial cell activation and are involved in the pathogenesis of TAO.Thus,understanding these molecular mechanisms to develop strategies for mitigating endothelial cell activation or injury is crucial for the treatment of TAO.
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