Targeting non-coding RNAs in unstable atherosclerotic plaques: Mechanism, regulation, possibilities, and limitations

Area of Science:

• Cardiovascular Research
• Molecular Biology
• Genetics

Background:

• Cardiovascular diseases (CVDs) are the leading global cause of death, primarily driven by arteriosclerosis and unstable atherosclerotic plaques.
• Plaque rupture leads to thrombosis, causing life-threatening events like strokes and myocardial infarctions.
• Current treatments focus on plaque stability, but effective strategies remain limited.

Purpose of the Study:

• To comprehensively review the regulatory mechanisms of atherosclerotic plaque rupture susceptibility.
• To discuss limitations of current therapeutic approaches for plaque instability.
• To highlight the clinical potential of non-coding RNAs (ncRNAs) in managing CVDs.

Main Methods:

• Literature review of existing research on atherosclerosis and non-coding RNAs.
• Analysis of pathophysiological processes involved in plaque formation and progression.
• Evaluation of current therapeutic strategies and their limitations.

Main Results:

• Atherosclerotic plaque progression involves complex interactions including cell apoptosis, lipid disorders, inflammation, and cell migration.
• Non-coding RNAs (ncRNAs) significantly influence vascular cell functions and atherosclerotic plaque development.
• Emerging evidence points to ncRNAs' role in regulating plaque stability.

Conclusions:

• ncRNAs are critical regulators of atherosclerotic plaque stability and rupture susceptibility.
• ncRNAs show promise as diagnostic biomarkers for CVD risk stratification.
• Targeting ncRNAs may offer novel therapeutic strategies to improve plaque stability and reduce cardiovascular events.