Exploring the role of curcumin in anti-atherosclerosis: Mechanisms and pathways of action.

BACKGROUND

Atherosclerosis (AS), a chronic inflammatory disease, remains a leading cause of cardiovascular morbidity. Curcumin, the primary bioactive compound from Curcuma longa, has demonstrated potent anti-atherosclerotic properties in preclinical studies, yet a comprehensive synthesis of its multi-targeted mechanisms is warranted.

PURPOSE: This review aims to systematically consolidate the molecular mechanisms by which curcumin inhibits the development and progression of atherosclerosis, providing a foundation for its clinical translation.

METHODS

A structured literature search was conducted in PubMed and Web of Science to identify studies elucidating the anti-atherosclerotic effects of curcumin. Key findings on its molecular targets and pathways were extracted and synthesized.

RESULTS

Curcumin exerts its anti-atherosclerotic effects through pleiotropic mechanisms. It potently suppresses vascular inflammation by inhibiting key pathways like nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK), and mitigates oxidative stress by activating the Nrf2/HO-1 axis. Curcumin improves lipid metabolism by reducing cholesterol synthesis and promotes reverse cholesterol transport. Furthermore, it inhibits vascular smooth muscle cell (VSMC) proliferation and migration, enhances endothelial function, and stabilizes plaques. Emerging evidence also highlights its role in modulating epigenetic markers (e.g., DNA methylation, histone acetylation) and reshaping gut microbiota homeostasis, which contribute to its protective effects.

CONCLUSION

Curcumin is a promising multi-targeted agent against atherosclerosis, impacting a wide spectrum of pathological processes from inflammation and oxidative stress to epigenetics and the gut-vascular axis. While preclinical evidence is compelling, well-designed clinical trials are crucial to definitively establish its efficacy and safety in human patients.