Background: Targeting PCSK9 by maintaining hemodynamic shear stress stability has been shown in several studies to reduce LDL-C, arterial plaque formation, and PCSK9 expression in atherosclerotic cardiovascular disease. Genome editing with CRISPR-associated regularly interspersed short palindromic repeats (CRISPR/Cas9) have therapeutic potential for atherosclerotic cardiovascular disease. This study aims to evaluate the role of CRISPR/Cas9 in targeting PCSK9 as an effective therapeutic and long-term effect on atherosclerotic vascular disease.
Methods: The method used in this study summarizes the article by looking for keywords that have been determined in the title and abstract. The authors used official guidelines from Science Direct, PubMed, the American College of Cardiology, Google Scholar, and PERKI to select full-text articles published within the last decade, prioritizing searches within the last five years.
Results: CRISPR/Cas9 deletion of PCSK9 in mouse models reduces LDL-C, Plaque accumulation in the arteries, and PCSK9 expression. Furthermore, CRISPR/Cas9 deletion in PCSK9 saves the stability of Hemodyanimc shear stress to control the PCSK9 expression that causes Atherosclerotic cardiovascular disease.
Conclusion: PCSK9 targeting by CRISPR/Cas9 deletion effectively reduces LDL-C, plaque buildup in the arteries, and PCSK9 expression. However, more research is needed to determine its side effects and safety.