ArticleJournal of the American Heart Association2025
Calbindin 2 as a Novel Biomarker and Therapeutic Target for Abdominal Aortic Aneurysm: Integrative Analysis of Human Proteomes and Genetics.
Article in Journal of the American Heart Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Multi-omics Mendelian randomization and machine learning identify candidate therapeutic targets for Alzheimer's and Parkinson's diseases.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAbdominal aortic aneurysm (AAA) is a clinical life-threatening issue. No pharmacological treatments are currently approved for the prevention and treatment of AAA. Therefore, identifying novel biomarkers and therapeutic targets is crucial for improving AAA management and outcomes.
methodsTo identify plasma proteins with potential causal effects on AAA, we integrated genetic evidence from proteome-wide Mendelian randomization, genetic correlation, and colocalization analysis. The role of identified proteins in AAA was further explored through the phenome-wide association study and mediation analysis. Multiomics data analysis, including bulk RNA sequencing, single-cell/single-nucleus RNA sequencing, and spatial transcriptomics, was employed to characterize the expression patterns of these proteins. Experimental validation was performed using an AAA model in apolipoprotein E-deficient mice infused with angiotensin II. Druggability analysis was conducted to identify drug candidates, which were tested in preclinical mouse models.
resultsCALB2 (calbindin 2) was identified as having a causal effect on AAA and may influence the progression of AAA through the regulation of lipid metabolism. Multiomics analysis revealed that CALB2 is predominantly expressed in the mesothelial cells of adipose tissues. Inhibition of CALB2 in an AAA mouse model alleviated AAA progression. Druggability analysis identified lenalidomide and genistein as potential therapeutic candidates, and experiments confirmed their efficacy in preventing AAA development.
conclusionsThis study identifies CALB2 as being associated with an increased risk of AAA and suggests that i might be a novel biomarker and therapeutic molecule for AAA management. Lenalidomide and genistein hold promising potential as treatments for patients with AAA.
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