To determine whether folate treatment, besides decreasing homocysteine (tHcy), improves coagulation status, oxidative stress and endothelial dysfunction and whether these depend on genetic polymorphism of the enzyme methylenetetrahydrofolate reductase (MTHFR).
A slight chronic hypoperfusion or an endothelial dysfunction associated with unfavorable genetic variations such as methylenetetrahydrofolate reductaseC677T variation and angiotensin-converting enzyme I/D polymorphism then may lead indirectly to a malfunction of the molecular cross-talk between the nucleus and the mitochondria.
Angiotensin-converting enzyme (ACE) insertion (I)/deletion (D) and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphisms are linked to endothelial dysfunction and to cerebral white matter lesions.
We aimed to investigate the relationships between serum asymmetric dimethyl arginine (ADMA), LOX-1, and Apelin-13 levels, which are known to act over nitric oxide with endothelial dysfunction and cardiac morphology as well as with each other in hemodialysis patients.
Genetic variants in endothelial nitric oxide synthase gene (NOS3) leading to endothelial dysfunction may be predispose to the coronary slow-flow phenomenon (CSFP).
The underlying causes of endothelial dysfunction with sex hormone deficiency are unknown but may be related to endothelial nitric oxide synthase dysfunction and oxidative stress.
The presence of sEng did not significantly affect the expression of selected members of TGF-β signaling (membrane endoglin, TGFβRII, ALK-5, ALK-1, Id-1, PAI-1 and activated Smad proteins-pSmad 1,5 and pSmad 2,3), inflammation, heart remodeling (PDGFb, Col1A1) and endothelial dysfunction (VCAM-1, ICAM-1) in the hearts of Sol-Eng+ mice compared to control mice on both chow and high-fat diet.
Nitric oxide (NO) plays critical role in endothelial dysfunction and oxidative stress in COPD, pointing to the significance of endothelial nitric oxide synthase gene (eNOS) variants.
Canonical NALP3 inflammasome activation is a caspase-1 medicated process, resulting in the secretion of IL-18 and IL-1β which lead to endothelial dysfunction.
Low sodium intake is paradoxically associated with adverse cardiovascular outcomes in individuals with type 2 diabetes mellitus (T2D), possibly from renin-angiotensin-aldosterone system (RAAS) activation, leading to endothelial dysfunction.
We also assessed whether these two MTHFR gene polymorphisms may be implicated in the development of cardiovascular (CV) events and subclinical atherosclerosis manifested by the presence of endothelial dysfunction, in a series of Spanish patients with RA.
Impaired circadian blood pressure variation in normotensive normoalbuminuric type 2 diabetes patients is associated with ACE DD genotype and marked endothelial dysfunction when compared to diabetic subjects with normal blood pressure rhythm.
In this work, we have studied whether NOS3 gene, previously related to endothelial dysfunction, might have a role in metabolic syndrome susceptibility in hypertensive patients.
Considering the relationships of apolipoprotein E(ApoE) polymorphism with LDL cholesterol (LDL-C) levels and coronary risk, it is possible that it brings on susceptibility to endothelial dysfunction and atherogenesis seen on uremia.
We followed up 212 randomly selected, nonobese, nondiabetic, insulin-sensitive participants in a population-based study without NAFLD or metabolic syndrome at baseline who were characterized for the common SREBF-1c gene rs11868035 A/G polymorphism, dietary habits, physical activity, adipokine profile, C-reactive protein (CRP), and circulating markers of endothelial dysfunction.
An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D, angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOSG894T variants are associated with an endothelial dysfunction (ED).
An increasing body of evidence suggests that different genetic factors, such as angiotensin-converting enzyme (ACE) I/D, angiotensin II type-1 receptor (AT1R) A1166C, methylenetetrahydrofolate reductase (MTHFR) C677T and ENOS G894T variants are associated with an endothelial dysfunction (ED).
We investigated whether <i>n</i>-3 PUFA could reverse endothelial dysfunction in CKD by improving endothelial nitric oxide synthase (eNOS) function and oxidative stress.
C677T polymorphism in methylenetetrahydrofolate reductase gene (MTHFR) is a major determinant of hyperhomocysteinemia, which results in endothelial dysfunction.
In conclusion, the homozygous NOS III variant (GG) status does not seem to interact additively with the ACE homozygous DD genotype in determining flow-mediated vasodilation in individuals with established atherosclerosis and pre-existent endothelial dysfunction.
It was aimed to explain the association of the endothelial dysfunction, which is thought to play a role in the pathophysiology of CSX, with C677T polymorphism on MTHFR gene based on genetic basis.