Inflammation contributes to the atherogenic role of intermittent hypoxia in apolipoprotein-E knock out mice

Arnaud, Claire; Poulain, Laureline; Lévy, Patrick; Demattéis, Maurice

doi:10.1016/j.atherosclerosis.2011.07.122

Cited by 77 publications

(61 citation statements)

References 35 publications

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“…The rodent sleep apnoea model (i.e. rodents exposed to intermittent hypoxia) confirmed the detrimental role of hypoxia in OSA-associated vascular alterations; intermittent hypoxia increases aortic IMT in C57BL6 mice [5,6] and accelerates the development of atherosclerotic lesions in C57BL6 mice on a high cholesterol diet [7] and in atherosclerosis-prone apolipoprotein E-deficient (ApoE -/-) mice [8,9]. However, the direct relationship between sleep apnoea or intermittent hypoxia and its cardiovascular consequences is not fully elucidated.…”

Section: Introductionmentioning

confidence: 80%

“…We have shown that intermittent hypoxia induced vascular and systemic inflammation in nonobese C57BL6 [6] and ApoE -/- [9] mice, and noted that intermittent hypoxia also induced inflammatory alterations and morphological changes of EWAT, with histological features of brown adipose tissue [17]. Therefore, we hypothesised that intermittent hypoxia itself could induce EWAT remodelling, which could contribute to metabolic and vascular disorders, independently of any obesity.…”

Section: Introductionmentioning

confidence: 99%

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Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis

et al. 2013

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Obstructive sleep apnoea is a highly prevalent disease characterised by repetitive upper airway collapse during sleep leading to intermittent hypoxia. Cardiometabolic complications of sleep apnoea have been mostly attributed to intermittent hypoxia. These consequences could be mediated through intermittent hypoxia-related alterations of the visceral white fat, as it is recognised for playing an important role in inflammation, atherogenesis and insulin resistance.Epididymal adipose tissue alterations were investigated in 20-week-old nonobese male apolipoprotein Edeficient mice exposed to intermittent hypoxia (inspiratory oxygen fraction 5-21%, 60-s cycle, 8 h?day -1 ) or air for 6 weeks. These adipose tissue alterations, as well as metabolic alterations and aortic atherosclerosis, were then assessed in lipectomised or sham-operated mice exposed to intermittent hypoxia or air for 6 weeks.Intermittent hypoxia induced morphological (shrunken adipocytes), functional (increased uncoupling protein-1 expression) and inflammatory (increased macrophage recruitment and secretion of interleukin-6 and tumour necrosis factor-a) remodelling of epididymal adipose tissue. Hypoxic mice presented more severe dyslipidaemia and atherosclerosis lesions and developed insulin resistance. Epididymal lipectomy attenuated both intermittent hypoxia-induced dyslipidaemia and atherogenesis, but did not improve insulin sensitivity.Our results confirmed that the dyslipidaemic and proatherogenic effects of intermittent hypoxia are partly mediated through morphological, functional and inflammatory remodelling of visceral white fat, regardless of obesity. @ERSpublications Dyslipidaemic and proatherogenic effects of intermittent hypoxia are partly mediated by visceral white fat remodelling

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Section: Introductionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis

et al. 2013

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“…The mechanisms by which CIH accelerates atherosclerotic disease are unclear but may include hypertension, dyslipidemia, insulin resistance, systemic inflammation, and oxidative stress (6). In rodent models, CIH accelerates the progression of atherosclerosis in C57BL/6J mice on a high-cholesterol diet (9,10) and in ApoE-deficient mice (11,12) by inducing dyslipidemia (10) and systemic inflammation (11,(13)(14)(15).…”

Section: Measurements and Main Resultsmentioning

confidence: 99%

Chronic Intermittent Hypoxia Induces Atherosclerosis via Activation of Adipose Angiopoietin-like 4

Drager

Yao

Hernandez

et al. 2013

Am J Respir Crit Care Med

151

120

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“…In C57BL/6J mice fed on a high cholesterol diet, treatment with intermittent hypoxia induced atherosclerosis which was not observed in animals treated with control conditions [53]. Similarly, in atherosclerosis-prone apolipoprotein-E deficient mice (ApoE -/-), intermittent hypoxia led to a significant acceleration of the atherosclerotic process when using high-fat [54] or normal diet-fed animals [55]. Even in non-genetically modified animals fed with a normal diet, intermittent hypoxia led to early changes including downregulated endothelial Platelet endothelial cell adhesion molecule-1 (a marker of vascular remodelling) expression at the aortic and cardiac levels suggesting endothelial dysfunction or an early event of atherogenesis [56].…”

Section: Systemic Inflammationmentioning

confidence: 98%

“…Systemic inflammation plays a pivotal role in all stages of atherosclerosis in general [58] and hence, not surprisingly, it is also central in intermittent hypoxia-induced pathogenesis. ARNAUD et al [55] demonstrated that inflammation at systemic and vascular levels contributes to the intermittent hypoxia atherogenicity in the ApoE -/-mice. Various studies have addressed interactions between the vascular endothelium and inflammatory cells in OSA.…”

Section: Systemic Inflammationmentioning

confidence: 99%

Sleep apnoea and the heart

et al. 2013

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Sleep apnoea is associated with significant daytime functioning impairment and marked cardiovascular morbidities, leading to a significant increase in mortality. Sympathetic activation, oxidative stress and systemic inflammation have been shown to be the main intermediary mechanisms associated with sleep apnoea and intermittent hypoxia. There are now convincing data regarding the association between hypertension, arrhythmias, coronary heart disease, heart failure, increased cardiovascular mortality and sleep apnoea. This has been evidenced in sleep apnoea patients and is supported by experimental data obtained in intermittent hypoxia. Whether treating sleep apnoea enables chronic cardiovascular consequences to be reversed is not fully established as regard coronary heart disease, arrhythmias and heart failure. In this late condition, complex bidirectional relationships occur, with obstructive sleep apnoea being a risk factor for heart failure whilst central sleep apnoea mainly appears as a consequence of heart failure. It remains to be established in adequately designed studies, i.e. large randomised controlled trials, whether treating sleep apnoea can improve heart failure morbidity and mortality. @ERSpublications Sleep apnoea is associated with arrhythmias, coronary disease and heart failure through intermittent hypoxia http://ow.ly/ne19T

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Inflammation contributes to the atherogenic role of intermittent hypoxia in apolipoprotein-E knock out mice

Cited by 77 publications

References 35 publications

Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis

Visceral white fat remodelling contributes to intermittent hypoxia-induced atherogenesis

Chronic Intermittent Hypoxia Induces Atherosclerosis via Activation of Adipose Angiopoietin-like 4

Sleep apnoea and the heart

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