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. 2022 Feb 18;12(2):310. doi: 10.3390/life12020310

Table 3.

A summary of the molecular mechanisms of vitamin E in vascular diseases.

Pathological/Biological
Condition		 Effect Target Tissues Reference
Hemolysis ↑ membrane stability, ↓ phospholipid fluidity Blood [41]
Membranal instability Activates PLA2, regulates and forms complexes
with LysoPC		 Vascular endothelium [43]
Membrane apoptosis Regulates PXR and other heterodimeric nuclear
receptors’ expression		 Vascular endothelium [46]
Cell toxicity Interacts with DHA to regulate UGT1A1 mRNA
expression		 Vascular endothelium [46]
Hypercholesterolemia Interacts with DHA to regulate SCD levels that
improve lipid metabolism		 Arteries [46]
Cell apoptosis ↓ caspace-3 production Vascular endothelium [47]
Atherosclerosis ↑ Cu/Zn SOD, SOC production Vascular endothelium [48]
Inflammation ↓ cytokines IL-1β, IL-8, IL-6 Vascular endothelium [49]
Hypercholesterolemia, atherosclerosis ↓ CD36 expression, ↑ PPARγ-LXRα-ABCA1 pathway (in the presence of ox-LDL) which ↓ cholesterol and
× foam cells		 Arteries [51]
Atherosclerosis, hypercholesterolemia, hypertension × PKC, ↓ VSMC proliferation, protects endothelial NO release and vascular relaxation, × ox-LDL and PMA release Vascular endothelium, vascular muscles [30,52,53]
CVD caused from diabetes ↓ DAG by ↑ DAG kinase which × PKC Vascular endothelium [54]
Atherosclerosis,
inflammation		 × TNF-α which ↑ CTGF in VSMC Vascular muscles [56]
Atherosclerosis × phosphorylation of p47phox by PMA and PKC
results in × NADPH oxidase which ↓ O2− production and hence ↓ ox-LDL		 Vascular endothelium [58]
Atherosclerosis ↓ PKB/Akt production, which ↓ CD36 via the
ox-LDL/CD36/PKB/PPARγ pathway		 Vascular endothelium, vascular muscles [7,59]
Hypercholesterolemia, atherosclerosis,
hyperlipidemia		 × MUFA or PUFA peroxidation, regulates various
lipid mediators		 Arteries, vascular
endothelium		 [7,61]
Atherosclerotic lesions, arterial inflammation αTP ↓ CD36 expression, THP-1 monocyte
proliferation		 Arteries [63]
Hypercholesterolemia ↓ cholesterol synthesis by binding to TAP1/2/3 Arteries [64]
Atherosclerosis αTP modulates VEGF genes expression through the PI3K/Akt pathway which ↑ cell repair, wound
healing, vascular permeability, vasculogenesis,
angiogenesis, and × hypoxia		 Arteries [60,63,65]
VTE ↓ hazard, anticoagulation and ↓ platelet clotting Blood, lungs [67]
Thrombosis × platelet aggregation by × platelet-MNC interaction, PKC activity, PMA-mediated P-selectin expression Blood [68]
Inflammation, thrombosis ↓ ICAM-1 and VCAM-1, which ↓ blood cell adhesion to vessels, ↓ CD11b, VLA-4 Arteries, veins [5,70]
Thrombosis, hypertension ↑ PLA2 and cyclooxygenase-1, which ↑ prostacyclin, which in turn ↑ vasodilation and ↓ platelet aggregation Arteries, veins [5]
Atherosclerosis, hyperlipidemia ↓ platelet aggregation by ↓ LDL-initiated thrombin hormone production Arteries [74]

↑: increases/upregulates; ↓: reduces/downregulates; ×: suppresses; PLA2: phospholipase A2; LysoPC: lysophosphatidylcholine species; PXR: pregnane X receptor; DHA: docosahexaenoic acid; UGT1A1: DP-glucuronosyltransferase 1A1; SCD: stearoyl-CoA desaturase; SOD, SOC: superoxide dismutase, caspace; αTP: α-tocopherol phosphate; CD36: CD36 scavenger receptor; PKC: enzyme protein kinase C; VSMC: vascular smooth muscle cell; PKB/Akt: protein kinase B; O2−: superoxide anion; NO: nitric oxide; PMA: phorbol 12-myristate 13-acetate; DAG: diacylglycerol; TNF-α: tumor necrosis factor-α; CTGF: connective tissue growth factor; ox-LDL: oxidized low-density lipoprotein; MUFA/PUFA: unsaturated fatty acids; TAP1/2/3: tocopherol-associated proteins; VEGF: vascular endothelial growth factor; PI3K/Akt: phosphatidylinositol-3-kinase; VTE: venous thromboembolism; MNC: mononuclear cells; ICAM-1: intercellular cell adhesion molecule; VCAM-1: vascular cell adhesion molecule-1.