ANRIL and atherosclerosis

What is known and objective The 3.8-kb-long antisense non-coding RNA at the INK4 locus (ANRIL) is transcribed from the short arm of human chromosome 9 on P21 and is associated with malfunction of the vascular endothelium, vascular smooth muscle cell (VSMC) proliferation/migration/senescence/apoptosis, mononuclear cell adhesion and proliferation, glycolipid metabolism disorder and DNA damage. Hence, ANRIL plays an important role in atherogenesis. Moreover, genome-wide association studies (GWAS) have identified ANRIL as a biomarker that is closely related to coronary heart disease (CHD). The objective of this review was to discuss the pathological mechanism of ANRIL in atherosclerotic development and its significance as a predictor of cardiovascular disease. Methods Review of the PubMed, EMBASE and Cochrane databases for articles demonstrating the roles of ANRIL in the development of atherosclerotic diseases. Results and discussion The abnormal expression of ANRIL is linked to vascular endothelium injury; the proliferation, migration, senescence and apoptosis of VSMCs; mononuclear cell adhesion and proliferation; glycolipid metabolism disorder; DNA damage; and competing endogenous RNAs. Moreover, ANRIL accelerates the progression of CHD by regulating its single nucleotide polymorphisms (SNPs). What is new and conclusion Considering that ANRIL accelerates atherosclerosis (AS) development and is a risk factor for CHD, it is reasonable for us to explore an efficacious ANRIL-based therapy for AS in CHD.