Folic acid, also prevents calcification of the aortic valve?!European Heart Journal China Study

2022-04-27 0 By

Tetrahydrobiotrexate (BH4) is a key determinant of the biological function of endothelial nitric oxide synthase.On February 9th, wuhan xiehe hospital cardiac vascular surgery, ZheYi 2 hospital heart Cai Zhejun with such as published in the European heart journal, a study suggests, aortic valve calcification occurs, endothelial cell source of BH4 and GTP ring hydrolase (GCH1) decreased significantly, and folic acid can improve the bioavailability of BH4 to suppress aortic valve calcification.We also found that reduced BH4 from valvular endothelial cells promotes peroxynitrite formation, leading to tyrosine nitrosation of dynamin-associated protein 1 (DRP1) in valvular interstitial cells and osteoblast differentiation, ultimately leading to aortic valve calcification.This study showed significant reductions in plasma and aortic valve BH4 levels and BH4/ dihydrobiotrexate (BH2) ratios in patients with aortic valve calcification compared with control subjects.At the same time, two key enzymes in BH4 biosynthesis, GCH1 and dihydrofolate reductase (DHFR), were also significantly reduced.Endothelial cell specific gCH1-deficient apolipoprotein E knockout (ApoE−/−) mice fed a Western diet for 24 weeks significantly increased peak transvalvular flow rate and increased aortic valve leaf calcium deposition.In the valvular interstitial cells stimulated by oxidized LDL, the deficiency of BH4 in valvular endothelial cells resulted in increased peroxynitrite formation and increased 3-nitrotyrosine protein.In ApoE−/− mice, folic acid significantly inhibited aortic valve calcification by increasing DHFR production and improving BH4 biosynthesis.Source:Zongtao Liu, Nianguo Dong, Haipeng Hui, et al. Endothelial cell-derived tetrahydrobiopterin prevents aortic valve calcification. European Heart Journal, Many difficult and complicated cases, a doctor can only see once in his life