Table 1_Inverse association between the extracellular matrix protein Tenascin-X and concurrent abdominal aortic calcification in patients with primary aldosteronism.docx

Tenascin-X (TNX), an extracellular matrix molecule encoded by the TNXB gene, was selected as the core candidate and validated via aldosterone-exposed vascular smooth muscle cells (VSMCs) as well as aldosterone-intervened mice.</p>Results<p>In total, 38 DEPs were distinguished across the two patient cohorts, comprising 6 upregulated proteins and 32 proteins with lowered expression levels. Gene Ontology results illustrated these molecules predominantly reside within extracellular regions and take part in cellular adhesion and immune regulatory activities.

KEGG pathway enrichment further highlighted prominent enrichment within the extracellular matrix receptor interaction cascade. Markedly suppressed TNX expression was detected in aldosterone-treated VSMCs (P < 0.001). In mouse aortic specimens, merely a marginal declining tendency of TNX was observed, which failed to reach statistical significance (P = 0.054).</p>Conclusion<p>This proteomic study analyzes serum protein profiles in primary aldosteronism patients with and without abdominal aortic calcification, and identifies reduced serum TNX expression in PA patients complicated by abdominal aortic calcification.

Further cellular experiments and aldosterone-intervened mouse studies revealed downregulation or a downward trend of key candidate molecule TNX, providing partial preliminary experimental support for the proteomic-identified candidate TNX. This study offers new research ideas for subsequent mechanistic investigations into abdominal aortic calcification in patients with primary aldosteronism.</p>