ArticleFrontiers in physiology2025
Tissue metabolomics reveals metabolic dysregulation associated with intimal hyperplasia in arteriovenous fistula stenosis.
Article in Frontiers in physiology, 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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6 authors.
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Abstract
Objective: This study performed untargeted LC-MS metabolomics on venous tissues from maintenance hemodialysis patients undergoing arteriovenous fistula (AVF) reconstruction surgery. Methods: A total of six stenotic and six non-stenotic AVF tissues were analyzed. Paired samples were collected from stenotic AVF segments and non-stenotic regions (control group). Histological analysis revealed significant intimal hyperplasia in stenotic tissues (687.90 ± 149.00 μm vs. 286.70 ± 95.18 μm, P < 0.0001 by HE staining) and excessive collagen deposition (Masson staining). Results: Metabolomic profiling identified 802 metabolites, with 356 differentially expressed (VIP > 1, P < 0.05), predominantly lipids/lipid-like molecules. KEGG enrichment highlighted five dysregulated pathways (P < 0.01): Arginine/proline metabolism; Glycerophospholipid metabolism; ABC transporters; Choline metabolism in cancer; Retrograde endocannabinoid signaling. Six metabolites showed perfect diagnostic potential (AUC = 1.0): niacin, free carnitine, 3-hydroxynonyl-5,7-dienoylcarnitine, 3-methylheptanediylcarnitine, dec-7-enoylcarnitine, and γ-aminobutyric acid. Significant metabolite-clinical correlations included: Choline positively correlating with serum phosphorus (r = 0.62, P = 0.008); Carnitine associating with hemoglobin levels (r = 0.58, P = 0.012). Conclusion: This tissue-based metabolomics study defines specific metabolic disturbances driving AVF stenosis, proposing mechanistic insights and candidate biomarkers.
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