ANRIL's Epigenetic Regulation and Its Implications for Cardiovascular Disorders

J Biochem Mol Toxicol. 2024 Dec;38(12):e70076. doi: 10.1002/jbt.70076.

Abstract

Cardiovascular disorders (CVDs) are a major global health concern, but their underlying molecular mechanisms are not fully understood. Recent research highlights the role of long noncoding RNAs (lncRNAs), particularly ANRIL, in cardiovascular development and disease. ANRIL, located in the human genome's 9p21 region, significantly regulates cardiovascular pathogenesis. It controls nearby tumor suppressor genes CDKN2A/B through epigenetic pathways, influencing cell growth and senescence. ANRIL interacts with epigenetic modifiers, leading to altered histone modifications and gene expression changes. It also acts as a transcriptional regulator, impacting key genes in CVD development. ANRIL's involvement in cardiovascular epigenetic regulation suggests potential therapeutic strategies. Manipulating ANRIL and its associated epigenetic modifiers could offer new approaches to managing CVDs and preventing their progression. Dysregulation of ANRIL has been linked to various cardiovascular conditions, including coronary artery disease, atherosclerosis, ischemic stroke, and myocardial infarction. This abstract provides insights from recent research, emphasizing ANRIL's significance in the epigenetic landscape of cardiovascular disorders. By shedding light on ANRIL's role in cellular processes and disease development, the abstract highlights its potential as a therapeutic target for addressing CVDs.

Keywords: ANRIL; atherosclerosis; cardiovascular disorders; coronary artery disease; ischemic stroke; lncRNAs; myocardial infarction.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases* / genetics
  • Cardiovascular Diseases* / metabolism
  • Cyclin-Dependent Kinase Inhibitor p15 / genetics
  • Cyclin-Dependent Kinase Inhibitor p15 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Epigenesis, Genetic*
  • Humans
  • RNA, Long Noncoding* / genetics
  • RNA, Long Noncoding* / metabolism

Substances

  • RNA, Long Noncoding
  • CDKN2B antisense RNA, human
  • Cyclin-Dependent Kinase Inhibitor p15
  • Cyclin-Dependent Kinase Inhibitor p16
  • CDKN2B protein, human
  • CDKN2A protein, human