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21st World Congress on Heart Disease



Changyi Johnny Chen, M.D., Ph.D., Baylor College of Medicine, Houston, TX, USA


Cardiovascular diseases (CVD) including heart disease, stroke and other vessel-related diseases are the leading global cause of death, accounting for more than 17.3 million deaths per year, a number that is expected to grow to more than 23.6 million by 2030. Many traditional risk factors are associated with CVD including hypertension, smoking, hypercholesterolemia, diabetes, physical inactivity, unhealthy diet and obesity as well as family history. However, these factors cannot account for the entire risk for incident diseases. Many other potential risk factors have been identified such as aldosterone, autoantibodies, brain natriuretic peptide (BNP), fibrin D-dimer, Willebrand factor (vWF), trimethylamine-N-oxide (TMAO), homocysteine, C-reactive protein, antiretroviral therapy drugs, adipokines, soluble CD40L, nitrotyrosine, chlorotyrosine and serum uric acid. For example, several recent large clinical studies have confirmed that hyperuricemia is a significant and independent risk factor for CVD including hypertension, ischemic heart disease, and heart failure, after an extensive adjustment for almost all of the possible confounding conditions. Hyperuricemia contributes to the progression of CVD through oxidative stress, systemic inflammation, and endothelial dysfunction. We showed that the treatment with clinically relevant concentrations of uric acid caused the downregulation of endothelial nitric oxide synthase (eNOS) in human endothelial cells by a unique mechanism of MAPKs (p38 and EKR1/2)-mediated signal transduction and GATA4-mediated eNOS promoter inhibition. Hyperuricemia-related endothelial dysfunction has been observed in rats and humans. Accordingly, xanthine oxidoreductase (XOR) inhibitors improve endothelial functions. We showed that hyperuricemia of uricase-/- mice caused downregulation of eNOS in the mouse aorta; while new XOR inhibitors as well as Allopurinol successfully inhibited eNOS downregulation in uricase-/- mice. These studies may suggest new strategies to prevent and treat CVD.



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