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.