Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombin activatable fibrinolysis inhibitor (TAFI), a recently described inhibitor of fibrinolysis, has been hypothesized as playing a role in atherothrombosis. However, the evidence from retrospective studies, which have evaluated the role of TAFI in vascular risk, is conflicting. In a prospective cohort (the PRIME Study) of nearly 10 000 apparently healthy men recruited in France (Lille, Strasbourg, Toulouse) and Northern Ireland (Belfast), we measured baseline plasma concentration of TAFI antigen among 143 participants (81 from France and 62 from Ireland) who subsequently developed angina pectoris and among 286 age-matched participants who remained free of disease during the 5 years of follow-up. Genotyping of the Ala147Thr polymorphism located in the TAFI gene was performed using an allele specific PCR. In France, mean levels of TAFI were significantly higher at baseline among men who subsequently developed angina pectoris compared with their control subjects (119 versus 107 %; p = 0.02). The risk of future angina pectoris increased with increasing tertiles of TAFI (p = 0.02), such that men in the highest tertile at study entry had a 5-fold higher relative risk than those in the lowest tertile (95% confidence interval, 1.38 to 18.58) after controlling for the conventional cardiovascular risk factors. No such difference was observed in Northern Ireland. In France, Thr/Thr carriers of the Ala147Thr polymorphism were significantly more frequent in cases than in controls (p = 0.01) leading to a relative risk of angina pectoris of 2.7 (95%CI 1.2-5.8). Increase in plasma TAFI antigen levels is a risk factor for angina pectoris in France. Genotyping for the Ala147Thr polymorphism seems to be a reliable tool to assess the risk mediated by TAFI.
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PMID:Association between TAFI antigen and Ala147Thr polymorphism of the TAFI gene and the angina pectoris incidence. The PRIME Study (Prospective Epidemiological Study of MI). 1262 41

Rho-associated coiled-coil forming protein kinases (ROCKs), the downstream target proteins of RhoA, are ubiquitously expressed serine-threonine protein kinases. ROCKs have diverse cellular functions, e.g. smooth muscle contraction, actin cytoskeleton organization, cell adhesion, and gene expression. Accumulating evidence has revealed that ROCKs are substantially involved in cardiovascular disorders such as angina, cerebral ischemia, myocardial ischemia, and cardiac hypertrophy. So far, the significant relationship of ROCKs with endothelial function has been reported. ROCKs inhibition by statins or other selective inhibitors leads to the upregulation and activation of endothelial nitric oxide synthase, resulting in the reduction of vascular inflammation and atherosclerosis. Meanwhile, it has been also demonstrated that endogenous nitric oxide could inhibit RhoA/ROCK signaling pathway. Taken together, there might be critical crosstalk of ROCKs with endothelial function. In addition, we further focus on leukocyte ROCK activity as a surrogate marker in patients with atherosclerosis-related diseases. Indeed, leukocyte ROCK activity has been shown to be increased in atherosclerotic patients, indicating the possible usage of leukocyte ROCK activity as a surrogate marker similar to endothelial function evaluated by flow-mediated dilation. Here, we review concerning ROCK signaling pathway, especially focusing on the crosstalk of ROCKs with endothelial function.
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PMID:Striking crosstalk of ROCK signaling with endothelial function. 2260 93

An automated method based on a hyphenated SPE-LC-MS/MS configuration has been optimized for the determination of essential amino acids (threonine, valine, methionine, leucine, isoleucine, lysine, tryptophan, and phenylalanine) in human serum, with the aim of discriminating between different states of coronary artery disease. Validation in terms of sensitivity (detection limits below 28.0 ng on column) and precision (repeatability expressed as relative standard deviation below 6.0%) supports the suitability of the method for application to a cohort of 122 atherosclerosis patients confirmed by a catheterization test. The cohort was composed by 80 individuals diagnosed with stable angina and 42 patients who suffered from acute myocardial infarction (AMI). Both groups of individuals are differentiated by the occurrence of ischemia in AMI patients due to the formation of thrombi. The chemometric treatment of the data obtained by multivariate analysis of variance (MANOVA) allowed comparison between both groups of diagnosed patients. Therefore, amino acids whose serum levels were affected by ischemia have been identified. The contribution of risk factors such as obesity and hypercholesterolemia as well as the individuals' gender to the concentration of essential amino acids has also been studied.
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PMID:Determination of essential amino acids in human serum by a targeting method based on automated SPE-LC-MS/MS: discrimination between artherosclerotic patients. 2281 6

Rho-associated kinases ROCK1 and ROCK2 are serine/threonine kinases that are downstream targets of the small GTPases RhoA, RhoB, and RhoC. ROCKs are involved in diverse cellular activities including actin cytoskeleton organization, cell adhesion and motility, proliferation and apoptosis, remodeling of the extracellular matrix and smooth muscle cell contraction. The role of ROCK1 and ROCK2 has long been considered to be similar; however, it is now clear that they do not always have the same functions. Moreover, depending on their subcellular localization, activation, and other environmental factors, ROCK signaling can have different effects on cellular function. With respect to the heart, findings in isoform-specific knockout mice argue for a role of ROCK1 and ROCK2 in the pathogenesis of cardiac fibrosis and cardiac hypertrophy, respectively. Increased ROCK activity could play a pivotal role in processes leading to cardiovascular diseases such as hypertension, pulmonary hypertension, angina pectoris, vasospastic angina, heart failure, and stroke, and thus ROCK activity is a potential new biomarker for heart disease. Pharmacological ROCK inhibition reduces the enhanced ROCK activity in patients, accompanied with a measurable improvement in medical condition. In this review, we focus on recent findings regarding ROCK signaling in the pathogenesis of cardiovascular disease, with a special focus on differences between ROCK1 and ROCK2 function.
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PMID:The Function of Rho-Associated Kinases ROCK1 and ROCK2 in the Pathogenesis of Cardiovascular Disease. 2663 6