aortic aneurysm/hypoxie

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Polymorphisms of genes involved in the hypoxia signaling pathway and the development of abdominal aortic aneurysms or large-artery atherosclerosis.

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BACKGROUND The pathogenesis of aortic diseases, both aneurysmal and occlusive, is associated with the occurrence of local ischemic/hypoxic conditions, but the genetic factors that differentiate the predisposition to specific types of aortic diseases are largely unknown. In this study, the functional

Deletion of hypoxia-inducible factor-1α in myeloid lineage exaggerates angiotensin II-induced formation of abdominal aortic aneurysm.

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Hypoxia-inducible factor (HIF)-1α is a transcription factor that regulates various genes responding to hypoxic conditions. We previously reported that myeloid-specific activation of HIF-1α had protective effects on hypertensive cardiovascular remodelling in mice. However the role of myeloid lineage

Silencing of hypoxia inducible factor-1α gene attenuated angiotensin Ⅱ-induced abdominal aortic aneurysm in apolipoprotein E-deficient mice.

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We aimed to determine the effect of HIF-1α, the main regulatory subunit of the hypoxia inducible factor 1 (HIF-1), on the development of the abdominal aortic aneurysm (AAA). AAA was induced in ApoE(-/-) mice by angiotensinⅡ (AngⅡ) infusion. In vivo silencing of HIF-1α was achieved by transfection of

Hypoxia-Inducible Factor-1α in Smooth Muscle Cells Protects Against Aortic Aneurysms-Brief Report.

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The purpose of this study was to determine the role of smooth muscle cell-derived hypoxia-inducible factor-1α (Hif-1α) in the pathogenesis of aortic aneurysms. Control mice and smooth muscle cell-specific hypoxia-inducible factor-1α-deficient mice were infused with β-aminopropionitrile for 2 weeks

Hypoxia in abdominal aortic aneurysm supports a role for HIF-1α and Ets-1 as drivers of matrix metalloproteinase upregulation in human aortic smooth muscle cells.

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OBJECTIVE We sought to determine whether hypoxia is an initiating factor in the matrix metalloproteinase-2 (MMP-2) up-regulation observed in abdominal aortic aneurysm (AAA) and whether hypoxia-inducible factor-1α (HIF-1α) or Ets-1 are mediating factors. METHODS Human AAA and normal aorta were

Medial Hypoxia and Adventitial Vasa Vasorum Remodeling in Human Ascending Aortic Aneurysm.

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Human ascending aortic aneurysms characteristically exhibit cystic medial degeneration of the aortic wall encompassing elastin degeneration, proteoglycan accumulation and smooth muscle cell loss. Most studies have focused on the aortic media and there is a limited understanding of the importance of

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

Inhibition of hypoxia inducible factor-1α attenuates abdominal aortic aneurysm progression through the down-regulation of matrix metalloproteinases.

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Hypoxia inducible factor-1α (HIF-1α) pathway is associated with many vascular diseases, including atherosclerosis, arterial aneurysms, pulmonary hypertension and chronic venous diseases. Significant HIF-1α expression could be found at the rupture edge at human abdominal aortic aneurysm (AAA)

Hypoxia-inducible factor 1 in clinical and experimental aortic aneurysm disease.

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OBJECTIVE Mural angiogenesis and macrophage accumulation are two pathologic hallmarks of abdominal aortic aneurysm (AAA) disease. The heterodimeric transcription factor hypoxia-inducible factor 1 (HIF-1) is an essential regulator of angiogenesis and macrophage function. In this study, we

Inflammatory cell infiltrates, hypoxia, vascularization, pentraxin 3 and osteoprotegerin in abdominal aortic aneurysms - A quantitative histological study.

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Information about the tissue characteristics of abdominal aortic aneurysms (AAAs), some of which may be reflected in the serum, can help to elucidate AAA pathogenesis and identify new AAA biomarkers. This information would be beneficial not only for diagnostics and follow-up but also for potential

Intermittent hypoxia due to right atrial compression by an ascending aortic aneurysm.

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Two cases are described wherein right atrial compression from a dilated and elongated ascending aorta caused intermittent positional hypoxia. Extrinsic compression of the right atrium caused shunting though a patent foramen ovale.

Does laminated intraluminal thrombus within abdominal aortic aneurysm cause anoxia of the aortic wall?

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[The functional status of the brain in patients with abdominal aortic aneurysm].

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We performed electroencephalography to 11 patients with abdominal aortic aneurysm in order to investigate the functional status of the brain. The relative potency (RP) of the main rhythms (alpha, beta, teta and delta) was increased, as well as the beta/alpha activation ratio. The increase of

Platypnoea-orthodeoxia syndrome in association with an ascending aortic aneurysm.

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Platypnoea-orthodeoxia syndrome is a uncommon condition presenting with dyspnoea and cyanosis that are characteristically worse in the upright posture and improved by lying supine. We present the case of a patient with a thoracic aortic aneurysm and a patent foramen ovale who presented with

Possible involvement of myofibroblast in the development of inflammatory aortic aneurysm.

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To clarify the role of myofibroblasts in the development of inflammatory aortic aneurysm (IAA), 11 cases of IAA (69.2+/-8.59 years) were investigated immunohistochemically and were morphometrically compared with 12 age-matched cases of atherosclerotic abdominal aneurysm (AAA, 69.6+/-5.94 years). The

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