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

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Τίτλος: Inverse association between the extracellular matrix protein Tenascin-X and concurrent abdominal aortic calcification in patients with primary aldosteronism.
Συγγραφείς: Zhang R; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Aila M; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Zhu Q; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Saiding S; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Wang M; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Wu T; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Guo B; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Li N; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China., Luo Q; Hypertension Center of People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Hypertension Institute, National Health Committee Key Laboratory of Hypertension Clinical Research Key Laboratory of Xinjiang Uygur Autonomous Region, Hypertension Research Laboratory, Xinjiang Clinical Medical Research Center for Hypertension (Cardio-Cerebrovascular) Diseases, Urumqi, China.
Πηγή: Frontiers in endocrinology [Front Endocrinol (Lausanne)] 2026 Oct 01; Vol. 17, pp. 1900237. Date of Electronic Publication: 2026 Oct 01 (Print Publication: 2026).
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Frontiers Research Foundation] Country of Publication: Switzerland NLM ID: 101555782 Publication Model: eCollection Cited Medium: Print ISSN: 1664-2392 (Print) Linking ISSN: 16642392 NLM ISO Abbreviation: Front Endocrinol (Lausanne) Subsets: MEDLINE
Imprint Name(s): Original Publication: [Lausanne : Frontiers Research Foundation]
Ιατρικοί όροι (MeSH): Tenascin*/blood , Tenascin*/metabolism , Hyperaldosteronism*/complications , Hyperaldosteronism*/blood , Hyperaldosteronism*/metabolism , Hyperaldosteronism*/pathology , Aorta, Abdominal*/pathology , Aorta, Abdominal*/metabolism , Vascular Calcification*/blood , Vascular Calcification*/metabolism , Vascular Calcification*/pathology , Vascular Calcification*/etiology, Extracellular Matrix Proteins/metabolism ; Muscle, Smooth, Vascular/metabolism ; Biomarkers/blood ; Humans ; Animals ; Male ; Female ; Mice ; Middle Aged ; Proteomics ; Mice, Inbred C57BL
Περίληψη: 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 TNXB gene, was selected as the core candidate and validated via aldosterone-exposed vascular smooth muscle cells (VSMCs) as well as aldosterone-intervened mice.
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 (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).
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.
(Copyright © 2026 Zhang, Aila, Zhu, Saiding, Wang, Wu, Guo, Li and Luo.)
Competing Interests: The author(s) declared that this work was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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Contributed Indexing: Keywords: abdominal aortic calcification; hypertension; primary aldosteronism; proteomics; tenascin-X
Substance Nomenclature: 0 (Tenascin)
0 (tenascin X)
0 (Extracellular Matrix Proteins)
0 (Biomarkers)
Entry Date(s): Date Created: 20261017 Date Completed: 20261017 Latest Revision: 20261019
Update Code: 20261019
PubMed Central ID: PMC13668541
DOI: 10.3389/fendo.2026.1900237
PMID: 42889018
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1664-2392
DOI:10.3389/fendo.2026.1900237