RETRACTED ARTICLE: Differential Expression of LOXL1-AS1 in Coronary Heart Disease and its Regulatory Mechanism in ox-LDL-Induced Human Coronary Artery Endothelial Cell Pyroptosis

Objective Coronary heart disease (CHD) is a notable contributor to the burden of human health. Dysregulated long non-coding RNAs (lncRNAs) are implicated in the pathogenesis of CHD. This study investigated the expression pattern of lncRNA LOXL1-AS1 in CHD and its regulatory mechanism in oxidized low-density lipoprotein (ox-LDL)-induced human coronary artery endothelial cell (HCAEC) pyroptosis. Methods Serum was collected from 62 CHD patients and 62 healthy volunteers for the detection of LOXL1-AS1 expression. The value of LOXL1-AS1 in CHD diagnosis and major cardiovascular adverse event (MACE) prediction was analyzed using the ROC curve. LOXL1-AS1, miR-16-5p, and SNX16 expressions in ox-LDL-treated HCAECs were determined using RT-qPCR. NLPR3, cleaved-caspase-1, and GSDMD-N protein levels were measured using Western blot. IL-1β and IL-18 concentrations were measured using ELISA. The binding relationships between LOXL1-AS1 and miR-16-5p and miR-16-5p and SNX16 were verified. Functional rescue experiment was performed to verify the role of miR-16-5p in HCAEC pyroptosis. Results LOXL1-AS1 was highly expressed in CHD patients. LOXL1-AS1 had diagnostic value for CHD and predictive value for MACE occurrence. ox-LDL-treated HCAECs showed reduced viability, increased IL-1β and IL-18 concentrations, and elevated NLPR3, cleaved-caspase-1, and GSDMD-N levels. LOXL1-AS1 silencing promoted cell viability and reduced pyroptosis. LOXL1-AS1 bound to miR-16-5p and miR-16-5p targeted SNX16. Inhibition of miR-16-5p reversed the inhibitory effect of LOXL1-AS1 silencing on HCAEC pyroptosis. Conclusion LOXL1-AS1 was elevated in CHD patients with a good diagnostic value for CHD and predictive value for MACE. LOXL1-AS1 downregulated miR-16-5p expression by binding to miR-16-5p to enhance ox-LDL-induced HCAEC pyroptosis, which may be associated with upregulation of SNX16 transcription.