aortic aneurysm/protease

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Cysteine protease cathepsins and matrix metalloproteinases in the development of abdominal aortic aneurysms.

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Both cysteine protease cathepsins and matrix metalloproteinases are implicated in the pathogenesis of abdominal aortic aneurysms (AAAs) in humans and animals. Blood and aortic tissues from humans or animals with AAAs contain much higher levels of these proteases, and often lower levels of their

Inflammaging and proteases in abdominal aortic aneurysm.

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Abdominal aortic aneurysm (AAA) is an age-related disease resulting in aortic wall weakening and dilatation which may progress to the fatal point of abrupt aortic wall rupture. Chronic inflammation is a driving force in the pathogenesis of AAA and extracellular matrix (ECM) proteases are considered

Quantitative expression and localization of cysteine and aspartic proteases in human abdominal aortic aneurysms.

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Cysteine and aspartic proteases possess high elastolytic activity and might contribute to the degradation of the abdominal aortic aneurysm (AAA) wall. The aim of this study was to analyze, in detail, the proteases (cathepsins B, D, K, L and S, and inhibitor cystatin C) found in human AAA and healthy

Cysteine Protease Cathepsins in Atherosclerosis and Abdominal Aortic Aneurysm.

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Extracellular matrix remodeling is an important mechanism in the initiation and progression of cardiovascular diseases. Cysteine protease cathepsins are among the important proteases that affect major events in the pathogenesis of atherosclerosis and abdominal aortic aneurysm, including smooth

Reduced protease inhibitory capacity in patients with abdominal aortic aneurysms is reversed with surgical repair.

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BACKGROUND Abdominal aortic aneurysm (AAA) disease is a complex degenerative process that is associated with elevated proteolytic activity. This increased proteolytic activity may be linked to an imbalance in the protease regulatory mechanisms. We hypothesize that reduced AAA plasma inhibitory

Difference in matrix-degrading protease expression and activity between thrombus-free and thrombus-covered wall of abdominal aortic aneurysm.

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OBJECTIVE It has been suggested that the intraluminal thrombus of abdominal aortic aneurysms (AAAs) predisposes for AAA rupture. Here, we examined the possibility that the intraluminal thrombus influences expression and activity of matrix-degrading proteases in the AAA wall. RESULTS Twenty patients

Identification of potential proteases for abdominal aortic aneurysm by weighted gene coexpression network analysis

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Proteases are involved in the degradation of the extracellular matrix, which contributes to the formation of abdominal aortic aneurysm (AAA). To identify new disease targets in addition to the results of previous microarray studies, we performed next-generation sequencing (NGS) of the whole

Genetic approach to the role of cysteine proteases in the expansion of abdominal aortic aneurysms.

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BACKGROUND The elastinolytic cysteine proteases, including cathepsins S and K, are overexpressed at sites of arterial elastin damage. Cystatin C, an inhibitor of these enzymes, is expressed in arterial smooth muscle cells; an imbalance in cystatin C has been implicated in the aortic wall

Cysteine protease activity in the wall of abdominal aortic aneurysms.

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BACKGROUND Cysteine proteases are potent elastolytic enzymes and together with their inhibitor, cystatin C, have been linked with the growth of abdominal aortic aneurysms (AAAs). These enzymes and their inhibitors have previously been studied in AAAs, but comparisons have always been made with wall

Assessment of the role of pancreatic proteases in human abdominal aortic aneurysms and occlusive disease.

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Previous studies on the pathogenesis of abdominal aortic aneurysms have shown both elastase-like activity in the aortic wall and a decreased elastin content. The present study, using specific radioimmunoassays for pancreatic elastase 2 (IRE2) and cationic trypsin(ogen) (IRCT), investigates the

Activities of proteases in parietal thrombus of aortic aneurysm.

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Deterioration of the aortic wall resulting in formation of aneurysm may be evoked by increased activity of elastases, collagenases and lysosomal proteases. These enzymes come from macrophages and neutrophil granulocytes which are elements of the inflammatory reaction accompanying aneurysm. These

Pathogenesis of abdominal aortic aneurysms: microRNAs, proteases, genetic associations.

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Abdominal aortic aneurysm (AAA) disease is a common, morbid, and highly lethal pathology. Extraordinary efforts have been launched to determine the molecular and pathophysiological characteristics of AAAs. Although surgery is highly effective in preventing death by rupture for larger AAAs, no

Long Noncoding RNA Hypoxia-Inducible Factor-1 Alpha-Antisense RNA 1 Regulates Vascular Smooth Muscle Cells to Promote the Development of Thoracic Aortic Aneurysm by Modulating Apoptotic Protease-Activating Factor 1 and Targeting let-7g

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Background: Thoracic aortic aneurysm (TAA) is a severe threat that is characterized by the increased aortic diameter. The dysfunction of vascular smooth muscle cells (VSMCs) contributes to the formation of TAA. Previous research indicated

Protease activity in the multi-layered intra-luminal thrombus of abdominal aortic aneurysms.

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BACKGROUND Rupture of an abdominal aortic aneurysm (AAA) is the cause of death in approximately 2% of men above 65 years. Most AAAs contain an intra-luminal thrombus (ILT), which is a potential source of proteases capable of degrading the underlying aneurysm wall. The AAA wall covered by a thick ILT

Involvement of the mural thrombus as a site of protease release and activation in human aortic aneurysms.

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Acquired abdominal aortic aneurysms are usually associated with a mural thrombus through which blood continues to flow. Some early data suggest that aneurysmal evolution correlates with the biological activity of the thrombus. Our hypothesis was therefore that the thrombus could adsorb blood

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