ArticleFrontiers in endocrinology2026
Inverse association between the extracellular matrix protein Tenascin-X and concurrent abdominal aortic calcification in patients with primary aldosteronism.
Article in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Patients diagnosed with primary aldosteronism (PA) are at significantly increased risk of abdominal aortic calcification (AAC) and subsequent cardiovascular complications. Notably, abdominal aortic calcification is independently associated with adverse cardiovascular outcomes. However, to date, no serum proteomic profiling has been specially carried out in PA patients complicated with AAC, leaving an unaddressed research gap. This study was designed to identify serum differentially expressed proteins (DEPs) via DIA-based untargeted proteomics. Methods: In this translational research project, data-independent acquisition (DIA) mass spectrometry was utilized to contrast serum proteomic landscapes from two PA subgroups: patients presenting with AAC and those without the calcification lesion. GO and KEGG functional enrichment analyses were conducted to decode biological functions of screened DEPs. Tenascin-X (TNX), an extracellular matrix molecule encoded by the Results: 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 ( Conclusion: 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.
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