MiR-423-5p Inhibition Exerts Protective Effects on Angiotensin II-Induced Cardiomyocyte Hypertrophy

Area of Science:

• Cardiovascular Biology
• Molecular Cardiology
• MicroRNA Therapeutics

Background:

• Angiotensin II (Ang II) is a key peptide implicated in cardiac hypertrophy.
• MicroRNAs (miRNAs) are critical regulators in cardiovascular diseases.
• The role of miR-423-5p in Ang II-induced cardiac hypertrophy remains unclear.

Purpose of the Study:

• To investigate the role of miR-423-5p in Ang II-induced cardiomyocyte hypertrophy.
• To elucidate the underlying molecular mechanism involving miR-423-5p in cardiac remodeling.

Main Methods:

• Upregulation of miR-423-5p in Ang II-treated human cardiomyocytes (HCMs) was assessed.
• miR-423-5p knockdown was performed to evaluate its effect on hypertrophy and oxidative stress.
• Bioinformatics and luciferase reporter assays identified SUPT6H as a direct target of miR-423-5p.
• SUPT6H knockdown experiments were conducted to validate its role.

Main Results:

• miR-423-5p expression was significantly increased in Ang II-stimulated HCMs.
• Knockdown of miR-423-5p attenuated Ang II-induced cardiomyocyte hypertrophy and oxidative stress.
• SUPT6H was confirmed as a direct target gene of miR-423-5p.
• SUPT6H knockdown exacerbated Ang II-induced hypertrophy and oxidative stress, effects reversed by miR-423-5p inhibition.

Conclusions:

• miR-423-5p plays a crucial role in promoting Ang II-induced cardiomyocyte hypertrophy and oxidative stress.
• miR-423-5p knockdown demonstrates a protective effect against Ang II-induced cardiac hypertrophy.
• Modulating miR-423-5p and its target SUPT6H represents a potential therapeutic avenue for cardiac hypertrophy.