Selective inhibition of endothelial NF-κB signaling attenuates chronic intermittent hypoxia-induced atherosclerosis in mice

Song, Dongmei; Fang, Guoqiang; Mao, Sun‐Zhong; Ye, Xiaobing; Liu, Gang; Miller, Edmund J.; Greenberg, Harly; Liu, Shu Fang

doi:10.1016/j.atherosclerosis.2018.01.027

Cited by 52 publications

(33 citation statements)

References 44 publications

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“…hibition of the NF-κB transcription factor appears to be beneficial in reducing cardiovascular-related complications including cardiac hypertrophy (Yu et al, 2015), cardiac fibrosis (Wang et al, 2018) and atherosclerosis (Song et al, 2018). In parallel, the role of phenolic acids in regulating the NF-κB transcription factor has also been reported previously (Cichocki et al, 2010;Wang et al, 2018).…”

Section: The Role Of Inflammation In Cardiovascular Diseasesmentioning

confidence: 75%

Implication of dietary phenolic acids on inflammation in cardiovascular disease

Ali

Ahmad

Budin

et al. 2020

Reviews in Cardiovascular Medicine

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Section: The Role Of Inflammation In Cardiovascular Diseasesmentioning

confidence: 75%

Implication of dietary phenolic acids on inflammation in cardiovascular disease

Ali

Ahmad

Budin

et al. 2020

Reviews in Cardiovascular Medicine

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“…The effects of IH on inflammation are controversial. 24,25 However, LOX has been reported to inhibit inflammation. 26 Thus, in this study, the anti-inflammatory effect of IH in BAPN induced TAD mice may be attributed to increased expression of HIF-1a and LOX.…”

Section: Discussionmentioning

confidence: 99%

Intermittent Hypoxia Alleviates β-Aminopropionitrile Monofumarate Induced Thoracic Aortic Dissection in C57BL/6 Mice

Yang

Jiao

et al. 2020

European Journal of Vascular and Endovascular Surgery

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WHAT THIS PAPER ADDS Thoracic aortic dissection (TAD) is a life threatening cardiovascular disorder. Intermittent hypoxia (IH) triggers beneficial effects in multiple physiological systems, such as hypertension and coronary heart disease, in clinical and animal models. It was found that IH alleviates b-aminopropionitrile monofumarate induced TAD in C57BL/6 mice. Future studies should focus on the specific mechanism of thez protective role of IH and whether IH might be a treatment method for TAD. Objective: Thoracic aortic dissection (TAD) has a high mortality rate. Intermittent hypoxia (IH) triggers both harmful and beneficial effects in numerous physiological systems. The effects of IH on TAD development were explored in a mouse model. Methods: b-Aminopropionitrile monofumarate (BAPN) was used to induce TAD in C57BL/6 mice. Three week old male mice were treated with 1 g/kg/day BAPN in drinking water for four weeks and simultaneously subjected to IH (n ¼ 30) (21%e5% O 2 , 90 s/cycle, 10 h/day, IH þ BAPN group) or normoxia (n ¼ 30) (21% O 2 , 24 h/day, BAPN group). Human VSMCs (HUASMCs) exposed to IH (30 min, 5% O 2)/re-oxygenation (30 min, 21% O 2) cycles with a maximum of 60 min/cycle to detect the effect of IH on HIF-1a and LOX via HIF-1a-siRNA. Results: It was found that BAPN administration significantly increased the lumen size and wall thickness of aortas compared with the normal group, but was significantly reversed by IH exposure. Additionally, IH exposure significantly increased the survival rate of BAPN induced TAD (70% vs. 40%). Furthermore, IH exposure reduced BAPN induced elastin breaks and apoptosis of vascular smooth muscle cells. IH exposure also reversed BAPN induced upregulation of inflammation and extracellular matrix (ECM) degradation. Real time polymerase chain reaction (RT-PCR) confirmed that IH inhibited inflammation and ECM degradation related genes interleukin (IL)-1b, IL-6, cathepsin S (Cat S), and matrix metalloproteinase 9 (MMP-9), but upregulated the ECM synthesis related genes lysyl oxidase (LOX) and collagen type I alpha2 (Col1a2) compared with the BAPN group. In vitro results suggest that IH promotes the expression of LOX via HIF-1a. Conclusion: The results suggest that IH alleviates BAPN induced TAD in C57BL/6 mice.

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“…Several studies have indicated that the relationship of APRIL and NF-KB signaling pathway activation is one of a complex interactive, APRIL could induce inflammatory activation by the activation of NF-KB signaling pathway [15,16], and conversely, NF-KBdependent pathways can influence APRIL secretion [17,18]. A large body of evidence, including experimental and clinical studies, have demonstrated that the activation of NF-KB-dependent inflammatory pathways by intermittent hypoxia and reoxygenation in OSA may be an important molecular mechanism of cardiovascular complication [4,19,20]. Moreover, both RNA and protein expression of APRIL have been shown in human plaque lymphocytes and macrophages and plasma [37,38].…”

Section: Discussionmentioning

confidence: 99%

“…Current evidence suggests that APRIL could induce inflammatory activation by the activation of NF-KB signaling pathway [15,16], and conversely, NF-KB-dependent signaling pathways, in turn, can influence APRIL secretion [17,18]. The activation of NF-KB-dependent inflammatory pathways by intermittent hypoxia and reoxygenation in OSA may be an important molecular mechanism of cardiovascular complication [4,19,20]. In addition, several studies showed that monocyte chemotactic protein-1 (MCP-1) and Lselectin as inflammation mediators can be regulated via the activation of NF-KB signaling pathways, and they were significantly elevated in patients with OSA [21][22][23][24].…”

mentioning

confidence: 99%

Plasma APRIL as a Potential Biomarker in the Diagnosis of Obstructive Sleep Apnea

Wen

Sun

Yang

et al. 2020

Preprint

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Background: Obstructive sleep apnea (OSA) is the most common type of sleep breathing disorder and is characterized by chronic intermittent hypoxia, which could cause inflammation and NF-KB-dependent inflammatory pathways activation. Circulating APRIL might play an important role in promoting inflammation and NF-KB-dependent inflammatory pathways activation. We explored the role of APRIL as a potential mechanism of inflammation in OSA patients. Methods: After detailed sleep evaluated, venous blood and demographic data were collected from 155 subjects with varying severity of OSA and 52 control subjects. Plasma levels of APRIL were measured by human Magnetic Luminex assay. Results: Plasma APRIL levels were significantly higher in OSA subjects compared with control subjects. Categorization of the OSA subjects into mild, moderate, and severe OSA subgroups showed that plasma levels of APRIL increased with severity. After adjusting confounding factors, found that increased plasma APRIL levels were conferred a higher odds ratio (OR) of OSA. Moreover, plasma APRIL levels were positively associated with the apnea-hypopnea index. Furthermore, plasma APRIL showed higher discriminatory accuracy in predicting the presence of OSA. Conclusions:Plasma APRIL levels were significantly associated with the occurrence of OSA and its severity. APRIL could be a plasma biomarker with a positive diagnostic value for inflammation and NF-KB–dependent inflammatory pathways activation in subjects with OSA.

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Selective inhibition of endothelial NF-κB signaling attenuates chronic intermittent hypoxia-induced atherosclerosis in mice

Cited by 52 publications

References 44 publications

Implication of dietary phenolic acids on inflammation in cardiovascular disease

Implication of dietary phenolic acids on inflammation in cardiovascular disease

Intermittent Hypoxia Alleviates β-Aminopropionitrile Monofumarate Induced Thoracic Aortic Dissection in C57BL/6 Mice

Plasma APRIL as a Potential Biomarker in the Diagnosis of Obstructive Sleep Apnea

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