ArticleApplied biochemistry and biotechnology2026
Expression of Chitosanase-3-like Protein 1 in Outflow Tract Veins of Patients with Autologous Arteriovenous Fistula Failure and Potential Involvement with Phenotypic Transformation of Medial Smooth Muscle Cells.
Article in Applied biochemistry and biotechnology, 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
objectiveChitosanase-3-like protein (CHI3L1) serum levels are expressed at elevated levels in Autologous arteriovenous fistula (AVF) dysfunction patients. This study was to investigate the expression and possible mechanisms of CHI3L1 in vascular tissues of AVF dysfunction patients.
methodsCollect healthy venous tissue from the head of uremic patients undergoing their first AVF surgery (control group) and non-functional fistula tissue from patients undergoing reconstructive surgery after AVF dysfunction (a total of 6 paired samples). The pathological characteristics of the tissues were observed using HE staining and EVG staining. CHI3L1 and M2 macrophage secreted factors (TGF-β1, PDGF, MMP2 and MMP9) proteins were analyzed by immunoblotting. The expression and localization of myofibroblast marker protein α-SMA and M2 macrophage marker protein CD206 were assessed by immunofluorescence labeling.
resultsThe lumen of the failed fistula tissues was significantly narrowed, with significant thickening of the venous intima and elastic fiber breakage compared with the control group. CHI3L1, TGF-β1, PDGF, MMP2 and MMP9 in the failed fistula tissues was significantly higher than that in the control group (P < 0.01). α-SMA and CD206 expression in the failed fistula tissues was significantly increased and clustered in the intima. Both α-SMA and CD206 in the intima were co-localized with CHI3L1.
conclusionCHI3L1 is highly expressed in dysfunctional fistula tissue, coexisting with M2 macrophage markers and α-SMA-positive cells. This suggests it may influence the proliferation, migration, and phenotypic transformation of medial smooth muscle cells by interacting with M2 macrophages and their secreted factors, thereby contributing to the development and progression of AVF dysfunction.
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