Evidence for activation of nuclear factor kappaB in obstructive sleep apnea

Yamauchi, Motoo; Tamaki, Shinji; Tomoda, Koichi; Yoshikawa, Masayuki; Fukuoka, Atsuhiko; Makinodan, Kiyoshi; Koyama, Noriko; Suzuki, Takahiro; Kimura, Hiroshi

doi:10.1007/s11325-006-0074-x

Cited by 78 publications

(41 citation statements)

References 27 publications

(29 reference statements)

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“…NF-kB is the master regulator of an inflammatory response and numerous inflammatory genes, such as TNF-a, IL-8 or ICAM-1, which are also known to be pro-atherogenic, are under its control. NF-kB activation has been demonstrated in cardiovascular tissue from mice treated with intermittent hypoxia and in cultured monocytes from OSA patients [61,62]. Using a cell culture model of intermittent hypoxia, RYAN et al [63] demonstrated a preferential activation of NF-kB-dependent proinflammatory pathways by intermittent hypoxia over adaptive hypoxia-inducible factor (HIF)-1 mediated pathways, which is in contrast to sustained hypoxia where adaptive pathways predominate.…”

Section: Systemic Inflammationmentioning

confidence: 99%

Sleep apnoea and the heart

Lévy

Ryan

Oldenburg

et al. 2013

European Respiratory Review

108

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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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Section: Systemic Inflammationmentioning

confidence: 99%

Sleep apnoea and the heart

Lévy

Ryan

Oldenburg

et al. 2013

European Respiratory Review

108

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“…Activation of transcription factors in OSAHS and in animal models of IH NF-kB and AP-1 Activation of inflammatory pathways by upregulation of NFkB was demonstrated in neutrophils and monocytes of patients with OSAHS [84][85][86], and in an in vitro model of HeLa cells treated with IH [87]. Consequently, upregulation of adhesion molecules and inflammatory cytokines and adipocytokines, the gene products of NF-kB, were also noted, further supporting activation of NF-kB in OSAHS [57,67,88,89], as well as in associated conditions and comorbidities [90].…”

Section: Ros As Signalling Moleculesmentioning

confidence: 99%

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Lavie¹,

Lavie²

2009

European Respiratory Journal

320

223

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Obstructive sleep apnoea/hypopnoea syndrome (OSAHS) is a highly prevalent breathing disorder in sleep that is an independent risk factor for cardiovascular morbidity and mortality. A large body of evidence, including clinical studies and cell culture and animal models utilising intermittent hypoxia, delineates the central role of oxidative stress in OSAHS as well as in conditions and comorbidities that aggregate with it. Intermittent hypoxia, the hallmark of OSAHS, is implicated in promoting the formation of reactive oxygen species (ROS) and inducing oxidative stress. The ramifications of increased ROS formation are pivotal. ROS can damage biomolecules, alter cellular functions and function as signalling molecules in physiological as well as in pathophysiological conditions. Consequently, they promote inflammation, endothelial dysfunction and cardiovascular morbidity. Oxidative stress is also a crucial component in obesity, sympathetic activation and metabolic disorders such as hypertension, dyslipidaemia and type 2 diabetes/insulin resistance, which aggregate with OSAHS. These conditions and comorbidities could result directly from the oxidative stress that is characteristic of OSAHS or could develop independently. Hence, oxidative stress represents the common underlying link in OSAHS and the conditions and comorbidities that aggregate with it.

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“…In addition, these alterations can turn on nuclear transcriptional factors, including nuclear factor-B, which induce production of inflammatory mediators, intracellular and vascular cell adhesion molecules [12] . All the above could facilitate vascular endothelial damage and atherogenesis [13][14][15] . In this way, intermittent hypoxia may lead to atherosclerosis and, ultimately, the cardiovascular consequences of OSAS.…”

Section: Activationmentioning

confidence: 99%

Obstructive sleep apnea syndrome and cardiovascular disease: The influence of C-reactive protein

Bouloukaki¹,

Mermigkis²,

Kallergis³

et al. 2015

WJEM

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Obstructive sleep apnea syndrome (OSAS) is a common medical condition, associated with atherosclerosis and cardiovascular disease (CVD). The underlying pathophysiologic mechanisms of this association have not been completely understood and may be multifactorial in origin. A number of studies suggest that inflammatory processes have emerged critical in the pathogenesis of CVD in OSAS. A range of circulating inflammatory molecules has been identified and measured, with a view to assess inflammation and predict vascular damage risk, such as plasma cytokines, adhesion molecules, and C-reactive protein (CRP). CRP is a relevant marker worthy of further study, because not only is elevated in patients with OSAS, but also is rapidly becoming a risk factor for cardiac disease. Furthermore, in selected OSAS patients, aggressive treatment of the disorder may lead to retarding or even improvement of CVD progression. However, still there is a debate on the true correlation between CRP and OSAS, as well as the clinical effect of any reduction after OSAS treatment. Further research is required to define those OSAS patients who will have a considerable reduction with treatment, as well as to understand the significance of the interaction between cardiovascular risk factor and CRP reduction in patients with OSAS.

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Evidence for activation of nuclear factor kappaB in obstructive sleep apnea

Cited by 78 publications

References 27 publications

Sleep apnoea and the heart

Sleep apnoea and the heart

Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link

Obstructive sleep apnea syndrome and cardiovascular disease: The influence of C-reactive protein

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