Literature DB >> 31703157

ANRIL and atherosclerosis.

Li Chen1, Hua Qu2, Ming Guo3, Ying Zhang3, Yuanyuan Cui3, Qiaoning Yang3, Ruina Bai3, Dazhuo Shi3.   

Abstract

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.
© 2019 John Wiley & Sons Ltd.

Entities:  

Keywords:  ANRIL; atherosclerosis; biomarker; mechanism

Mesh:

Substances:

Year:  2019        PMID: 31703157     DOI: 10.1111/jcpt.13060

Source DB:  PubMed          Journal:  J Clin Pharm Ther        ISSN: 0269-4727            Impact factor:   2.512


  18 in total

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