Molecular mechanisms of the intracranial aneurysms and their association with the long noncoding ribonucleic acid - A review of literature.

Long noncoding ribonucleic acids (RNAs) are important regulators of gene expression. Antisense noncoding RNA in the INK4 locus (ANRIL), which was coded on the Chr9p21.3 loci, participates in the pathogenesis of tumor, coronary artery disease, type 2 diabetes mellitus, and other diseases. A genome-wide association study indicated ANRIL to be a candidate gene that may lead to the development of an intracranial aneurysm (IA) formation. However, the detailed molecular mechanisms are unknown and have not been studied. Through reviewing the molecular mechanisms responsible for the development of IA and the regulation pathway of ANRIL, this paper presents four possible molecular mechanisms that may be responsible for the influence of ANRIL on the development of IAs, that is, cell cycling, Krüppel-like factor 2 (KLF2), caspase recruitment domain family member 8, and retinoid metabolism. ANRIL may become a molecular marker or therapeutic target of IA in the future. To the best of our knowledge, this is the first paper elucidating the molecular linkage between ANRIL and IAs.