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Fig. 2 | Biomarker Research

Fig. 2

From: Therapeutic potential of folic acid supplementation for cardiovascular disease prevention through homocysteine lowering and blockade in rheumatoid arthritis patients

Fig. 2

Mechanisms explaining homocysteine-related cardiovascular diseases at large. Dark arrow main mechanisms; dotted arrow minor mechanism. HHcy Hyperhomocysteinemia; NO nitric oxide; DNA deoxyribonucleic acid; ADMA asymmetric dymethyl arginine; ox-LDL oxidized low density lipoprotein cholesterol; CVD cardiovascular diseases. Through S-nitrosohomocysteine, ADMA and oxidative stress, HHcy reduces NO bioavailability, thus causing endothelial dysfunction. Under high propensity for coagulation (characterized by platelet adhesion and activation, production of clotting molecules, impaired fibrinolysis) that can be exacerbated by HHcy, endothelial dysfunction evolves towards atherothrombosis. Besides, HHcy-related oxidative stress increases ox-LDL production hence leading to formation of the atheromatous plaque which together with arterial smooth muscle cells proliferation trigger atherosclerosis. Atherosclerosis and atherothrombosis (completed atherosclerosis with ruptured plaque and thrombosis) lead to CVD

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Biomarker Research

ISSN: 2050-7771

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