Atherosclerosis is a lipid-driven chronic inflammatory disease that poses a serious threat to health. Legumain (LGMN), also known as asparagine endonuclease, is a new type of cysteine proteases that can specifically hydrolyze substrate molecules containing asparagine residues. It has anti-apoptotic effects in mammals and plays an antigen-presenting role in inflammatory response. Several studies have found that LGMN can activate multiple signal pathways to promote cell apoptosis and migration, inflammatory response, and the development of atherosclerosis. Importantly, LGMN exerts pro-atherogenic effects by participating in a variety of pathophysiological mechanisms of atherosclerosis, including vascular remodeling, inflammatory response, plaque stability, and the degradation of extracellular matrix. In the present review, we describe the LGMN distribution, structure, generation, and functional partners. Furthermore, we summarize the relationship between LGMN and atherosclerosis. Based on the relationship between LGMN and atherosclerosis, LGMN may be a potential biomarker for atherosclerosis.
Keywords: atherosclerosis; inflammation; legumain; plaque stability; vascular remodeling.
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