Anti-Atherosclerotic Mechanisms of Dietary Polyphenols

Dietary polyphenols encompass a diverse family of plant-derived compounds that exert atheroprotective effects through multiple complementary pathways. Central to their action is the mitigation of oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defences, such as through activation of the Nrf2–HO-1 axis. Polyphenols also preserve endothelial function by inhibiting proinflammatory signalling cascades, reducing adhesion molecule expression and restoring nitric oxide bioavailability. In the arterial intima, these agents impede uptake of oxidised low-density lipoprotein by macrophages, limit foam cell formation and promote reverse cholesterol transport via enhanced expression of cholesterol efflux transporters. Furthermore, several polyphenols activate Sirtuin1, a deacetylase that fosters autophagy and suppresses vascular inflammation, thereby stabilising plaque architecture. Collectively, these mechanisms converge to slow lesion initiation and progression, offering nutritional avenues to complement conventional lipid-lowering and anti-inflammatory therapies.

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Anti-Atherosclerotic Mechanisms of Dietary Polyphenols publication trend

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Technical terms

Polyphenols: Plant-derived compounds with multiple phenolic rings that confer antioxidant and signalling-modulating properties.

Atherosclerosis: Chronic arterial disease characterised by lipid deposition, inflammatory cell infiltration and plaque formation.

Endothelial dysfunction: Impaired vascular endothelium marked by reduced nitric oxide bioavailability and heightened inflammatory activation.

Foam cells: Lipid-laden macrophages that accumulate within arterial walls and drive plaque development.

Oxidised LDL (ox-LDL): Modified low-density lipoprotein that promotes macrophage uptake and inflammatory signalling.

Autophagy: Cellular process for degradation and recycling of damaged organelles and proteins, important for vascular homeostasis.

Sirtuin1 (SIRT1): NAD⁺-dependent deacetylase that regulates metabolism, stress responses and autophagy.

Nrf2: Transcription factor that induces expression of antioxidant and cytoprotective genes.

HO-1 (Heme oxygenase-1): Enzyme induced by Nrf2 that degrades haem to biliverdin, carbon monoxide and iron, with antioxidant effects.

References

1. Natural Sirtuin1 Activators and Atherosclerosis: an Overview. Current Atherosclerosis Reports (2023).
2. Quercetin Suppresses the Progression of Atherosclerosis by Regulating MST1-Mediated Autophagy in ox-LDL-Induced RAW264.7 Macrophage Foam Cells. International Journal of Molecular Sciences (2019).
3. Kaempferol Protects Blood Vessels From Damage Induced by Oxidative Stress and Inflammation in Association With the Nrf2/HO-1 Signaling Pathway. Frontiers in Pharmacology (2020).