Review Article

CRISPR/Cas9 Tool for MicroRNAs Editing in Cardiac Development, Function, and Disease

Author(s): Leila Abkhooie and Shirin Saberianpour*

Volume 12, Issue 1, 2023

Published on: 03 November, 2022

Page: [13 - 21] Pages: 9

DOI: 10.2174/2211536611666220922092601

Price: $65

Abstract

CRISPR/Cas9 is a powerful gene-editing technology. Extensive scientific data exist that the CRISPR/Cas9 system can target small, non-coding, active RNA molecules, including microRNAs (miRNAs). miRNAs have been recognized as key regulators of different cell biological processes, such as the modulation of fibrosis and cardiac hypertrophy, as well as the regulation of cardiomyocytes. Also, it has been demonstrated that miRNAs strongly affect organ evolution, and that the concentration of miRNAs can involve the differentiation, development, and function of different organs. In addition, the current findings clearly indicate that miRNAs can select and control their targets based on their concentrations. CRISPR/Cas9 genome-editing technology is a stronger system for stopping miRNAs than previous methods, including antisense inhibitors. CRISPR/Cas9 tools can be used to eliminate small areas of DNA and determine miRNA in cases where similar groups of miRNAs are in the same strand. Herein, besides other emerging strategies, we critically summarize the recent investigations linking miRNA-targeted therapeutics and CRISPR/Cas9 system to clarify and combine different delivery platforms and cell-fate engineering of miRNAs function and miRNA-based therapeutic intervention in cardiac development, function, and disease. Based on our findings from the literature, it appears that the use of the CRISPR/Cas technology provides new perspectives for understanding the molecular mechanism of cardiovascular disease and can be effective in treating and controlling cardiac development, function, and disease in the future.

Keywords: CRISPR/Cas9, MicroRNAs, cardiac development, gene editing techniques, cytoplasm, organ evolution.

Graphical Abstract
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