Targeting the epigenome in in-stent restenosis: from mechanisms to therapy

Molecular Therapy: Nucleic Acids

Yonghong Li¹  Yuanyuan Meng²  Tao Yu²  Panyu Yang²  Junjie Guo³  Xi Yang³  Xin Liu³  Yanyan Yang⁴  Min Li⁵  Lynn Htet Htet Aung⁵ 

[1] Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, No. 38 Dengzhou Road, Qingdao 266021, People’s Republic of China;Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, No. 16 Jiangsu Road, Qingdao 266000, People’s Republic of China;Department of Cardiology, The Affiliated Hospital of Qingdao University, Road No. 59 Haier, Qingdao 266100, Shandong, People’s Republic of China;Department of Immunology, School of Basic Medicine, Qingdao University, No. 308 Ningxia Road, Qingdao 266071, People’s Republic of China;Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, No. 38 Dengzhou Road, Qingdao 266021, People’s Republic of China;

关键词: in-stent restenosis;    epigenetics;    DNA methylation;    histone modification;    non-coding RNAs;    target therapy;   

DOI  :  

来源: DOAJ

【 摘 要 】

Coronary artery disease (CAD) is one of the most common causes of death worldwide. The introduction of percutaneous revascularization has revolutionized the therapy of patients with CAD. Despite the advent of drug-eluting stents, restenosis remains the main challenge in treating patients with CAD. In-stent restenosis (ISR) indicates the reduction in lumen diameter after percutaneous coronary intervention, in which the vessel’s lumen re-narrowing is attributed to the aberrant proliferation and migration of vascular smooth muscle cells (VSMCs) and dysregulation of endothelial cells (ECs). Increasing evidence has demonstrated that epigenetics is involved in the occurrence and progression of ISR. In this review, we provide the latest and comprehensive analysis of three separate but related epigenetic mechanisms regulating ISR, namely, DNA methylation, histone modification, and non-coding RNAs. Initially, we discuss the mechanism of restenosis. Furthermore, we discuss the biological mechanism underlying the diverse epigenetic modifications modulating gene expression and functions of VSMCs, as well as ECs in ISR. Finally, we discuss potential therapeutic targets of the small molecule inhibitors of cardiovascular epigenetic factors. A more detailed understanding of epigenetic regulation is essential for elucidating this complex biological process, which will assist in developing and improving ISR therapy.

【 授权许可】

Unknown