aortic valve stenosis/protease

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Ubiquitin-specific Protease as the Underlying Gene Biomarker for Aortic Stenosis

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ass="sub-title">Background: Aortic stenosis is a common heart valvular disease whose pathological processes include an inflammatory reaction and lipid accumulation. However, its detailed pathogenesis is yet to be completely elucidated. Therefore, it is of great significance to

Changes in von Willebrand factor-cleaving protease (ADAMTS-13) in patients with aortic stenosis undergoing valve replacement or balloon valvuloplasty.

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It was the objective of this study to determine whether reduced cleavage of von Willebrand factor (VWF) multimers following aortic valve replacement (AVR) is a consequence of reduced shear stress or postoperative changes in VWF cleavage protease (ADAMTS-13) activity. Aortic stenosis (AS) may be

Effect of propranolol on the activity of neutral, alkaline and acidic proteases in rat myocardium after aortic stenosis.

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The aim of the study was to investigate the effect of propranolol upon the activity of proteases in rat myocardium subjected to aortic stenosis. In acute heart hypertrophy induced by aortic stenosis, the activity of all three proteases in the myocardium does not change significantly. Propranolol in

Modification of the secretion pattern of proteases, inflammatory mediators, and extracellular matrix proteins by human aortic valve is key in severe aortic stenosis.

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One of the major challenges in cardiovascular medicine is to identify candidate biomarker proteins. Secretome analysis is particularly relevant in this search as it focuses on a subset of proteins released by a cell or tissue under certain conditions. The sample can be considered as a plasma

[Aortic stenosis and extracellular matrix remodeling].

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Valvular heart diseases represent an important public health burden. With the decrease in the incidence of rheumatic heart disease, calcific aortic stenosis has now become the most common valvular disease in Western countries. Its prevalence increases with age, such that its affects about 4% of the

Apolipoprotein A-I proteolysis in aortic valve stenosis: role of cathepsin S.

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Aortic valve stenosis (AVS) is the most common valvular heart disease in the Western world. Therapy based on apolipoprotein A-I (apoA-I), the major protein component of high-density lipoproteins, results in AVS regression in experimental models. Nevertheless, apoA-I degradation by proteases might

Beneficial Effects of High-Density Lipoproteins on Acquired von Willebrand Syndrome in Aortic Valve Stenosis.

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BACKGROUND Infusions of apolipoprotein A-I (apoA-I), the major protein component of high-density lipoproteins (HDL), result in aortic valve stenosis (AVS) regression in experimental models. Severe AVS can be complicated by acquired von Willebrand syndrome, a haemorrhagic disorder associated with

No evidence for increased intraoperative bleeding in aortic-valve stenosis: a comparative analysis of haemotherapy in 136 patients undergoing aortic-valve replacement.

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OBJECTIVE An association of aortic-valve stenosis and abnormal bleeding, particularly from gastrointestinal angiodysplasia, has been reported. In this setting, high-shear stress generated by the transvalvular gradient leads to a conformational change of plasmic von Willebrand factor, making this

A surgical case of aortic stenosis with recurrent gastrointestinal bleeding: Heyde syndrome.

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BACKGROUND The combination of aortic stenosis, acquired coagulopathy, and anemia due to gastrointestinal (GI) bleeding is described as Heyde syndrome. METHODS We report a surgical case of a 77-year-old man who was admitted because of melena and exertional chest compression. GI endoscopy could not

Structural and Histochemical Alterations in the Aortic Valves of Elderly Patients: A Comparative Study of Aortic Stenosis, Aortic Regurgitation, and Normal Valves.

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The aim of this study was to reveal the pathogenesis of aortic stenosis (AS) and regurgitation (AR) by comparing differences in mechanical and biochemical alterations. We applied scanning acoustic microscopy (SAM) to measure the speed of sound (SOS) through valves to estimate the elasticity and

Lymphangiogenesis in aortic valve stenosis--novel regulatory roles for valvular myofibroblasts and mast cells.

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OBJECTIVE To investigate mechanisms of lymphangiogenesis in aortic valve stenosis (AS). METHODS Lymphatic vessels were visualized with LYVE-1 staining in 20 control, 5 sclerotic, and 40 stenotic human aortic valves. Vascular endothelial growth factors (VEGFs) VEGF-C and VEGF-D, and their

Potential role of microRNA-10b down-regulation in cardiomyocyte apoptosis in aortic stenosis patients.

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MicroRNAs have been associated with cardiomyocyte apoptosis, a process involved in myocardial remodelling in aortic valve (Av) stenosis (AS). Our aim was to analyse whether the dysregulation of myocardial microRNAs was related to cardiomyocyte apoptosis in AS patients. Endomyocardial biopsies were

Molecular basis of calpain cleavage and inactivation of the sodium-calcium exchanger 1 in heart failure.

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Cardiac sodium (Na(+))-calcium (Ca(2+)) exchanger 1 (NCX1) is central to the maintenance of normal Ca(2+) homeostasis and contraction. Studies indicate that the Ca(2+)-activated protease calpain cleaves NCX1. We hypothesized that calpain is an important regulator of NCX1 in response to pressure

Effect of propranolol upon protein and proteolytic synthesis activity in hypertrophic myocardium.

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The aim of the study was to investigate the effect of propranolol upon protein synthesis and degradation processes in cell-free subfractions of rat myocardium in experimental cardiac hypertrophy induced by aortic stenosis. It was found that hypertrophy stimulates incorporation of 3H-amino acids by

Corin-deficient W-sh mice poorly tolerate increased cardiac afterload.

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C57BL/6-Kit(W-sh/W-sh) mice are generally regarded as a mast cell-deficient model, as they lack the necessary kit receptor for mast cell development. Further characterization of this strain, however, indicates that C57BL/6-Kit(W-sh/W-sh) mice also have a disruption in the Corin gene. Corin is a

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