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Endothelial dysfunction is a pivotal contributor to atherosclerosis (As) pathogenesis. A comprehensive understanding of the mechanisms of endothelial dysfunction would provide novel insights into effective treatment of As. Recent advances in genome and transcripome technology have enabled researchers to further explore the molecular mechanisms of endothelial dysfunction. It has been found that the regulatory network of competitive endogenous RNA (ceRNA) mediated by long non-coding RNA (lncRNA) plays a key role in endothelial dysfunction. lncRNA acts as a “molecular sponge” for microRNA (miRNA) to block the post-transcriptional repression of miRNA on downstream target gene messenger RNA (mRNA) by binding to miRNA, thereby regulating the function and phenotypic conversion of endothelial cell (EC) lncRNA-miRNA-mRNA interactions are widely involved in play an essential role EC inflammatory responses, apoptosis, autophagy, angiogenesis, and endothelial-mesenchymal transition (EndMT). Which suggests that it may be a potential therapeutic targets for As.