https://www.selleckchem.com/products/etomoxir-na-salt.html Thus, we discuss gene therapy as the most promising approach for treating FXS in the near future.Critical roles of several microRNAs have been implicated in atherosclerosis (AS). In this study, we studied the functional role of miR-140-5p in AS. An AS model was constructed in THP-1 macrophages challenged with oxidized low-density lipoprotein (ox-LDL). The expression of miR-140-5p was up- or downregulated with corresponding mimic or inhibitor regents. Our experiments showed that the levels of cell apoptosis and fatty acid accumulation were decreased in THP-1 macrophages treated with miR-140-5p mimic, whereas increased in those treated with miR-140-5p inhibitor. The levels of ROS (reactive oxygen species), MDA (malondialdehyde), TC (Triglyceride), and TG (total cholesterol) were reduced and the level of SOD (superoxide dismutase) was improved in miR-140-5p overexpressed THP-1 macrophages, which can be reversed with miR-140-5p depletion. Moreover, through bioinformatics analysis, we found toll-like receptor 4 (TLR4) was a potential target of miR-140-5p. Luciferase reporter assay demonstrated that miR-140-5p regulated TLR4 expression via binding 3'UTR of TLR4 in THP-1 macrophages. In ox-LDL challenged THP-1 macrophages, the expression of TLR4 was decreased after miR-140-5p mimic transfection, whereas improved after treatment with miR-140-5p inhibitors. As a conclusion, miR-140-5p can participate in inhibiting ox-LDL-induced oxidative stress and cell apoptosis via targeting TLR4 in macrophage-mediated ox-LDL induced AS.Excessive release of neutrophil extracellular traps (NETs) is associated with disease severity and contributes to tissue injury, followed by severe organ damage. Pharmacological or genetic inhibition of NET release reduces pathology in multiple inflammatory disease models, indicating that NETs are potential therapeutic targets. Here, we demonstrate using a preclinical basket approach that our thera