Identification and Validation of CCL3 as an Inflammation‑Related Biomarker for Arteriovenous Fistula Dysfunction

Objective To investigate the key inflammation‑related genes associated with arteriovenous fistula (AVF) dysfunction and to identify and validate their associations with AVF dysfunction, thereby providing new directions and a theoretical basis for the prevention, diagnosis, and treatment of AVF dysfunction. Methods Bioinformatics analysis and the GeneCards database were used to screen for inflammation‑related differentially expressed genes (DEGs) associated with AVF dysfunction, and C‑C motif chemokine ligand 3 (CCL3) was identified as a candidate gene. Immune infiltration analysis was performed to explore the association between CCL3 and various immune cell types. Subsequently, CCL3 expression in clinical samples and its relationship with clinical parameters were validated. Results (1) A total of 64 inflammation‑related DEGs were identified through bioinformatics screening, with CCL3 emerging as a potential key gene associated with AVF dysfunction. (2) Immune infiltration analysis revealed that CCL3 was positively correlated with activated mast cells, monocytes, and neutrophils, and negatively correlated with resting mast cells. (3) Both intimal thickness and the intima‑to‑media thickness ratio were significantly greater in the AVF dysfunction group compared to the initial AVF group. (4) Immunohistochemical staining showed that CCL3 expression was significantly higher in the AVF dysfunction group than in the control group. Furthermore, CCL3 expression was positively correlated with intimal thickness and the intima‑to‑media thickness ratio, whereas no significant correlations were observed with clinical parameters such as age, albumin, or hemoglobin. Conclusion This study demonstrates that CCL3 is highly expressed in venous tissues of patients with AVF dysfunction, supporting its potential as an inflammation-related biomarker for the diagnosis and management of AVF dysfunction.