atherosclerosis/hypoxia

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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

Potential Role of mRNAs and LncRNAs in Chronic Intermittent Hypoxia Exposure-Aggravated Atherosclerosis.

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Atherosclerosis is the pathological basis of cardiovascular disease. Obstructive sleep apnea (OSA) aggravates atherosclerosis, and chronic intermittent hypoxia (CIH) as a prominent feature of OSA plays an important role during the process of atherosclerosis. The mechanisms of CIH in the development

Intermittent Hypoxia Composite Abnormal Glucose Metabolism-Mediated Atherosclerosis In Vitro and In Vivo: The Role of SREBP-1.

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Objective

The aim of this study was to establish a 3T3-L1 adipocyte model and ApoE^-/- mouse model of intermittent hypoxia (IH) composite abnormal glucose metabolism (AGM) in vitro and in vivo and explore their synergistic damage effect leading to

Sleep apnoea inducing hypoxemia is associated with early signs of carotid atherosclerosis in males.

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The intima-media thickness (IMT) of carotid arteries as a marker of preclinical atherosclerosis was measured by ultrasonography in 49 subjects to determine, how strongly the obstructive sleep apnoea (OSA) syndrome is associated with atherosclerosis. Maximal IMT was higher in patients with

Endothelial hypoxia induction of atherosclerosis: an explanation of patency rates for internal mammary artery and other coronary artery bypass grafts.

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The major etiological factors of atherosclerosis are reviewed and the case strengthened for endothelial hypoxia being the major initiator. Hypoxia is also shown to be the major cause of coronary artery bypass graft occlusions. The pathophysiological differences between pedicle and free arterial

Non-ischemic hypoxia of the arterial wall is a primary cause of atherosclerosis.

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The response-to-injury hypothesis has been the dominant model of atherosclerosis for 20 years. However, it does not explain the experimental role of oxygen in atherogenesis, does not explain many of the clinical features of atherosclerosis, and has failed to provide useful countermeasures. I propose

Hypoxia and atherosclerosis: re-evaluation of an old hypothesis.

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It was hypothesized over 40 years ago that a decrease in the oxygenation of the vascular wall might somehow be involved in atherogenesis. Recent studies concerning the mechanism of oxygenation indicate that diffusion through plasma is of major importance, meaning that a moderate, prolonged hypoxia

NF-κB and hypoxia: a double-edged sword in atherosclerosis.

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This Commentary highlights the article by Fang et al, which describes novel mouse models of chronic intermittent hypoxia (CIH)-induced atherosclerosis, revealing that loss of the NF-κB p50 subunit increased atherosclerosis in the presence of CIH.

Chronic hypoxia accelerates the progression of atherosclerosis in apolipoprotein E-knockout mice.

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The aim of this study was to investigate the effect of chronic hypoxia on the development and progression of atherosclerosis in apolipoprotein E-knockout (apoE-KO) mice. Male and female apoE-KO mice (6 weeks old) and age- and sex-matched wild-type mice were kept under hypoxic conditions (10.0 +/-

Expression of hypoxia-inducible angiogenic proteins (hypoxia-inducible factor-1alpha, vascular endothelial growth factor, and E26 transformation-specific-1) and plaque hemorrhage in human carotid atherosclerosis.

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OBJECTIVE Plaque hemorrhage in carotid atherosclerosis promotes plaque progression, resulting in cerebrovascular disease. Hypoxia inducible factor-1alpha (HIF-1alpha) induces angiogenesis via the expression of vascular endothelial growth factor (VEGF) and E26 transformation-specific-1 (Ets-1). The

Diabetic atherosclerosis: is there a role for the hypoxia-inducible factors?

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Atherosclerosis is a major cause of mortality worldwide and is driven by multiple risk factors, including diabetes. Diabetes is associated with either an insulin deficiency in its juvenile form or with insulin resistance and obesity in Type 2 diabetes mellitus, and the latter is clustered with other

Intermittent Hypoxia and Hypercapnia Accelerate Atherosclerosis, Partially via Trimethylamine-Oxide.

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Obstructive sleep apnea (OSA) is a common disorder characterized by intermittent hypoxia and hypercapnia (IHC) during sleep. OSA has been shown to be a risk factor for atherosclerosis, but the relation of IHC to the induction or progression of atherosclerosis is not well understood. To dissect the

Docosahexaenoic acid supplementation modifies fatty acid incorporation in tissues and prevents hypoxia induced-atherosclerosis progression in apolipoprotein-E deficient mice.

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The n-3 polyunsaturated fatty acid, docosahexaenoic acid (DHA), displays anti-inflammatory properties that may prevent atherosclerosis progression. Exposure of apolipoprotein-E deficient (ApoE(-/-)) mice to chronic intermittent hypoxia (CIH) accelerates atherosclerosis progression. Our aim was to

Tet3 enhances IL-6 expression through up-regulation of 5-hmC in IL-6 promoter in chronic hypoxia induced atherosclerosis in offspring rats.

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Tet1, Tet2, and interleukin-6 (IL-6) have been linked to atherosclerosis. Whether Tet3 has a relationship with atherosclerosis and IL-6 was unknown. This study aims to determine the link between Tet3 and IL-6, and the role of Tet3 in prenatal hypoxia-induced atherosclerosis in

Chronic intermittent hypoxia induces atherosclerosis by NF-κB-dependent mechanisms.

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Chronic intermittent hypoxia (CIH) causes atherosclerosis in mice fed a high cholesterol diet (HCD). The mechanisms by which CIH promotes atherosclerosis are incompletely understood. This study defined the mechanistic role of NF-κB pathway in CIH+HCD induced atherosclerosis. Wild type (WT) and mice

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