Research Progress on the Effect and Mechanism of Gene Transfection in Reducing the Inflammatory Response of Atherosclerosis.

INTRODUCTION

Gene transfection techniques have potential therapeutic value in reducing the inflammatory response in atherosclerosis. Atherosclerosis is a chronic inflammatory disease. Its pathological process involves multiple types of cells and signaling pathways.

METHODS

In recent years, researchers have used gene transfection techniques to introduce specific genes into vascular or immune cells in order to inhibit inflammatory responses, stabilize plaques, and slow down the process of atherosclerosis. Research progress has shown that gene transfection can exert anti-inflammatory effects through various mechanisms. IL-10 transfection suppresses atherosclerosis by activating the STAT3 pathway, reducing TNF-α and IL-6 expression in macrophages. Conversely, eNOS transfection enhances nitric oxide bioavailability, inhibiting endothelial cell adhesion molecule expression (e.g., VCAM-1) and monocyte recruitment.

RESULTS

Other studies have regulated the expression of inflammation-related genes by transfecting miRNA (tiny RNA), thus inhibiting the inflammatory response of atherosclerosis.

DISCUSSION: Despite preclinical efficacy, clinical translation is hindered by suboptimal vector tropism (e.g., viral vectors exhibit off-target hepatotoxicity) and immune-mediated clearance of non-viral vectors (e.g., liposomes trigger complement activation). Long-term risks of insertional mutagenesis (retroviral vectors) and epigenetic silencing of transgenes further limit durability.

CONCLUSION

This paper discusses the role and mechanism of gene transfection in reducing the inflammatory response in atherosclerosis.