
circFOXO3 facilitated endothelial cell senescence and atherosclerosis through binding to HnRNPK


With the development of the social economy and an increasingly aging population, cardiovascular diseases have become a severe threat to public health. Vascular aging is a primary risk factor for the development of cardiovascular diseases and it is associated with the cellular senescence of the vascular endothelium.1 Endothelial cell senescence leads to endothelial dysfunction that manifests as impaired endothelium-dependent vasorelaxation and vascular inflammation, ultimately predisposing individuals to atherosclerosis and other cardiovascular complications.2 By delaying senescence of vascular endothelial cells, it is possible to reduce or prevent the occurrence and development of atherosclerosis.
