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. 2020 Jun 10;21(11):4149. doi: 10.3390/ijms21114149

Figure 1.

Figure 1

The summary of the potential mechanisms by which n-3 polyunsaturated fatty acids (n-3 PUFAs) supplementation may modulate endothelial function. Several possible targets by which n-3 PUFAs supplementation modulate endothelial function are: (a) increasing production of endothelium nitric oxide (NO), (b) reducing formation or increasing elimination of reactive oxygen species (ROS), (c) decreasing vascular or systemic inflammation (e.g., endothelial activation and endothelium–leukocyte interaction), (d) inducing angiogenesis/neovascularization and mobilization of bone-marrow derived endothelial progenitor cells (EPCs), and (e) increasing the expression and/or activity of other endothelium-derived vasodilators (e.g., eicosanoids). A—arachidonic acid; AChIR—acetylcholine induced relaxation; BH4—tetrahydrobiopterin; BH2—7,8-dihydrobiopterin; DHA—docosahexaenoic acid; eNOS—endothelial nitric oxide synthase; EPA—eicosapentaenoic acid; ICAM—1-intercellular adhesion molecule 1; n-3 PUFAs—n-3 polyunsaturated fatty acids; SDF-1α—stromal cell-derived factor 1; sLEx—Sialyl Lewisx; VCAM-1—vascular cell adhesion molecule 1; VEGF—vascular endothelial growth factor.