Gene Expression Analysis of Inflammation, Apoptosis, and DNA Repair Mechanisms in the Pathogenesis of Ankylosing Spondylitis

Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease characterized by persistent inflammation, oxidative stress, immune dysregulation, and abnormal bone remodeling. Recent evidence suggests that microRNA-mediated post-transcriptional regulation and DNA damage response pathways may contribute to AS pathogenesis. This study aimed to investigate the expression profiles of selected microRNAs and genes associated with inflammation, apoptosis, and DNA repair mechanisms in patients with AS. A total of 30 patients diagnosed with AS and 30 healthy controls were included in the study. Gene and microRNA expression levels, including miRNA-574-5p, miRNA-30c-5p, MDM2, RAD51, NFKB1, BAX, ERCC1, and ATR, were analyzed using quantitative real-time PCR (qRT-PCR). Inflammatory parameters, including C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and interleukin-6 (IL-6), were also evaluated. The results demonstrated significantly increased miRNA-574-5p expression and significantly decreased MDM2 expression in the AS group compared with controls (p<0.05). CRP and IL-6 levels were also significantly elevated in patients with AS. Logistic regression analysis identified miRNA-574-5p, MDM2, and CRP as independently associated with AS. Receiver operating characteristic (ROC) analysis revealed that miRNA-574-5p and MDM2 exhibited significant diagnostic performance for distinguishing AS patients from healthy individuals. Correlation analyses demonstrated a positive association between miRNA-574-5p and BAX, whereas a negative correlation was observed between miRNA-574-5p and ESR. These findings suggest that altered miRNA-574-5p and MDM2 expression may contribute to inflammatory activity, apoptosis, and cellular stress responses in AS. Overall, the findings suggest that altered miRNA-574-5p and MDM2 expression may be associated with ankylosing spondylitis and represent candidate molecular biomarkers that warrant further validation in larger independent cohorts.