ANRIL in Cardiovascular Diseases: Expression, Mechanism and Therapeutic Implications

Cardiovascular diseases (CVDs) remain a leading cause of global mortality, with pathogenesis driven by multifactorial processes including genetic susceptibility, metabolic dysregulation, angiogenesis, and inflammation. Long non-coding RNAs (lncRNAs) have been recognized as key modulators of gene expression in cardiovascular pathophysiology. Among them, the Antisense Non-coding RNA in the INK4 Locus (ANRIL)-mapping to the well-established CVD-associated chromosome 9p21 locus-has garnered substantial research interest. Initially identified in melanoma, ANRIL spans approximately 126.3 kb and comprises 19 exons, existing in both linear and circular isoforms with distinct functional profiles. This review systematically outlines the dysregulation of ANRIL expression across seven major cardiovascular conditions and elucidates the isoform-specific mechanisms through which it contributes to disease progression, integrating recent advances in this field. We further discuss emerging evidence suggesting a potential role of ANRIL in cardiac hypertrophy. In light of its involvement in diverse cardiovascular disorders, ANRIL represents a compelling candidate for therapeutic target and a promising biomarker, warranting further translational investigation.