CA1 significantly aggravats atherosclerosis and MTZ, a inhibitor of CA1, can alleviate the disease.

Aortic calcification is essential for atherosclerosis (AS). Carbonic anhydrase I (CA1) can promote calcification in aortic tissues to stimulate AS plaque formation, and methazolamide (MTZ), a CA inhibitor, can be used to treat AS by inhibiting CA1-mediated calcification. This study used an established a CA1 [+/+] KI Apoe [-/-] mice to confirm stimulatory role of CA1 on AS and the therapeutic effect of MTZ and investigate the mechanism. In this study, Apoe [-/-] mice with CA1 overexpression were induced to AS by administrating high-fat food. The present study confirmed that CA1 is AS-therapeutic target by mediating the proportions of B1/MZB-1 cells, CD8+T cells, CD11c+ macrophages and CD11c- macrophages as well as their AS-related gene expressions and focal adhesion pathway. MTZ can be used for AS therapy. Overall design: CA1 knockin ApoE-/- mice were fed a high-fat diet to establish an AS model and then treated with MTZ. The aortic tissues were analyzed using single-cell sequencing.