lncRNA SND1-IT1/miR-494-3p regulation in ox-LDL-induced endothelial cell injury: novel insights into coronary heart disease pathogenesis and diagnostic biomarkers.

OBJECTIVES: Coronary heart disease (CHD) is a major challenge in cardiovascular disease. This study investigated the role of lncRNA SND1-IT1 in oxidized low-density lipoprotein (ox-LDL)-induced injury of human umbilical vein endothelial cells (HUVECs). MATERIALS AND METHODS: Serum was collected from healthy individuals and CHD patients. SND1-IT1 and miR-494-3p expression was analyzed by RT-qPCR, with ROC curves evaluating diagnostic potential. HUVECs were exposed to ox-LDL to induce injury and transfected to modulate target molecule expression. Cell viability and apoptosis were assessed using CCK8 and flow cytometry. Inflammatory cytokines and antioxidant enzymes were assessed by ELISA. Molecular interactions were verified through dual-luciferase reporters and RIP. RESULTS: In CHD patients, SND1-IT1 expression was significantly elevated (1.29 ± 0.18) compared to healthy controls (1.00 ± 0.14, P < 0.001), while miR-494-3p expression was notably downregulated (0.72 ± 0.16 vs. 1.01 ± 0.15, P < 0.001). Their combined assessment provide effective diagnostic value for CHD occurrence. Ox-LDL damaged HUVECs by inhibiting viability, enhancing apoptosis, inflammation, oxidative stress, and cell adhesion. SND1-IT1 knockdown alleviated these ox-LDL-induced injuries. SND1-IT1 acts as a sponge for miR-494-3p, whose downregulation reversed the protective effects of SND1-IT1 silencing. ZBTB20 was identified as a direct target of miR-494-3p and was upregulated in ox-LDL-treated HUVECs, counteracting the beneficial effects of miR-494-3p upregulation. CONCLUSION: Altered SND1-IT1 and miR-494-3p expressions in CHD patients show potential as biomarkers for CHD risk assessment. SND1-IT1 may regulate ox-LDL-induced damage in HUVECs by modulating the interaction between miR-494-3p and ZBTB20.