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

GSE253001 Mus musculus Expression profiling by high throughput sequencing 4 samples Submitted 2026/01/19 Platform GPL24247
Summary
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.
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Direct links to NCBI, no account and no request form: the whole study as GSE253001_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 4 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1063626 and SRA study SRP483319. Searching any of these in the dataset finder brings you back here.

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