aortic rupture/protease

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Emphysema: A Potential Risk Factor for Subarachnoid Hemorrhage and Ruptured Aortic Aneurysm

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Background and Purpose- Protease/antiprotease imbalance is implicated in the pathogenesis of emphysema and may also lead to vessel wall weakening, aneurysm development, and rupture. However, it is unclear whether emphysema is associated with cerebral and aortic aneurysm rupture. Methods- We

Contained Aortic Rupture With Hematoma and Gastrointestinal Bleeding.

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CREB3 (Luman) is a family member of ER resident transcription factors, which are cleaved upon the induction of ER stress. Their N-terminal fragments shuttle into the nucleus where they regulate the transcription of target genes. Here, we found that human CREB3 is phosphorylated within its

Coagulation in aortofemoral bifurcation bypass grafting.

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Few data are available on the pathophysiology of the coagulation system during aortic surgery. Cross-clamping of the aorta, intestinal eventeration and circulatory shock in ruptured aortic aneurysms are thought to cause coagulation disturbances and hyperfibrinolysis. A prospective study of several

Loss of Timp3 gene leads to abdominal aortic aneurysm formation in response to angiotensin II.

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Aortic aneurysm is dilation of the aorta primarily due to degradation of the aortic wall extracellular matrix (ECM). Tissue inhibitors of metalloproteinases (TIMPs) inhibit matrix metalloproteinases (MMPs), the proteases that degrade the ECM. Timp3 is the only ECM-bound Timp, and its levels are

Serpina3n attenuates granzyme B-mediated decorin cleavage and rupture in a murine model of aortic aneurysm.

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Granzyme B (GZMB) is a proapoptotic serine protease that is released by cytotoxic lymphocytes. However, GZMB can also be produced by other cell types and is capable of cleaving extracellular matrix (ECM) proteins. GZMB contributes to abdominal aortic aneurysm (AAA) through an extracellular,

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