Omega-3 fatty acids: mechanisms underlying 'protective effects' in atherosclerosis

Abstract

Purpose of review: This article provides an updated review on mechanistic and molecular studies relating to the effects of n-3 fatty acids (FA) on inhibiting atherogenesis.

Recent findings: The effects of n-3 FA on modulating arterial lipoprotein lipase levels link to changes in lipid deposition in the arterial wall. Lipoprotein lipase expression in the arterial wall also relates to local macrophage-mediated inflammatory processes. Increasing evidence suggests that n-3 FA ameliorate inflammation, another key component in the development of atherosclerosis, including decreases in proinflammatory cytokine production. n-3 FA inhibit atherogenic signaling pathways and modulate the phenotypes of inflammatory leukocytes and their recruitment in the arterial wall.

Summary: New mechanistic insights into the antiatherogenic action of n-3 FA have emerged. These studies may contribute to future therapeutic advances in preventing mortality and morbidity associated with atherosclerosis.

Figure 1. Summary of potential “beneficial effects” of n-3 FA in atherosclerosis

n-3 FA modulate atherosclerosis by affecting uptake and binding of LDL to the arterial wall. This is associated with reduced arterial LpL and macrophage levels. n-3 FA are protective against inflammation in the arterial wall by reducing the production of pro-inflammatory cytokines in monocytes (MO), macrophages or dendritic cells (DC) and decreasing the recruitment of inflammatory leukocytes to the arterial wall, including neutrophils (NE) and MO. Lastly, n-3 FA and n-3-derived eicosanoids, resolvins and protectins are potential anti-inflammatory lipid mediators in atherosclerosis. Specific examples of pathways related to each area are shown in the square boxes.