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Yang, Chongzhe

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Yang

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Chongzhe

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Yang, Chongzhe
Author's Publications: search.filters.isAuthorOfPublication.6249e2f7-400c-4c5b-a02e-da60573de0e4

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    Allergic lung inflammation promotes atherosclerosis in apolipoprotein E-deficient mice
    (Elsevier BV, 2016) Liu, Cong-Lin; Wang, Yi; Liao, Mengyang; Santos, Marcela; Fernandes, Cleverson; Sukhova, Galina; Zhang, Jin-Ying; Cheng, Xiang; Yang, Chongzhe; Huang, Xiaozhu; Levy, Bruce; Libby, Peter; Wu, Gongxiong; Shi, Guo-Ping
    Inflammation drives asthma and atherosclerosis. Clinical studies suggest that asthmatic patients have a high risk of atherosclerosis. Yet this hypothesis remains uncertain, given that Th2 imbalance causes asthma whereas Th1 immunity promotes atherosclerosis. In this study, chronic allergic lung inflammation (ALI) was induced in mice by ovalbumin sensitization and challenge. Acute ALI was induced in mice by ovalbumin and aluminum sensitization and ovalbumin challenge. Atherosclerosis was produced in apolipoprotein E-deficient (Apoe–/–) mice with a Western diet. When chronic ALI and atherosclerosis were produced simultaneously, ALI increased atherosclerotic lesion size, lesion inflammatory cell content, elastin fragmentation, smooth muscle cell (SMC) loss, lesion cell proliferation, and apoptosis. Production of acute ALI before atherogenesis did not affect lesion size, but increased atherosclerotic lesion CD4+ T cells, lesion SMC loss, angiogenesis, and apoptosis. Production of acute ALI after atherogenesis also did not change atherosclerotic lesion area, but increased lesion elastin fragmentation, cell proliferation, and apoptosis. In mice with chronic ALI and diet-induced atherosclerosis, daily inhalation of a mast cell inhibitor or corticosteroid significantly reduced atherosclerotic lesion T-cell and mast cell contents, SMC loss, angiogenesis, and cell proliferation and apoptosis, although these drugs did not affect lesion area, compared with those that received vehicle treatment. In conclusion, both chronic and acute ALI promote atherogenesis or aortic lesion pathology, regardless whether ALI occurred before, after, or at the same time as atherogenesis. Anti-asthmatic medication can efficiently mitigate atherosclerotic lesion pathology.
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    Asthma Associates With Human Abdominal Aortic Aneurysm and RuptureSignificance
    (Ovid Technologies (Wolters Kluwer Health), 2016) Liu, Cong-Lin; Wemmelund, Holger; Wang, Yi; Liao, Mengyang; Lindholt, Jes S.; Johnsen, Søren P.; Vestergaard, Henrik; Fernandes, Cleverson; Sukhova, Galina; Cheng, Xiang; Zhang, Jin-Ying; Yang, Chongzhe; Huang, Xiaozhu; Daugherty, Alan; Levy, Bruce; Libby, Peter; Shi, Guo-Ping
    Objective—Both asthma and abdominal aortic aneurysms (AAA) involve inflammation. It remains unknown whether these diseases interact. Approach and Results—Databases analyzed included Danish National Registry of Patients, a population-based nationwide case–control study included all patients with ruptured AAA and age- and sex-matched AAA controls without rupture in Denmark from 1996 to 2012; Viborg vascular trial, subgroup study of participants from the population-based randomized Viborg vascular screening trial. Patients with asthma were categorized by hospital diagnosis, bronchodilator use, and the recorded use of other anti-asthma prescription medications. Logistic regression models were fitted to determine whether asthma associated with the risk of ruptured AAA in Danish National Registry of Patients and an independent risk of having an AAA at screening in the Viborg vascular trial. From the Danish National Registry of Patients study, asthma diagnosed <1 year or 6 months before the index date increased the risk of AAA rupture before (odds ratio [OR]=1.60–2.12) and after (OR=1.51–2.06) adjusting for AAA comorbidities. Use of bronchodilators elevated the risk of AAA rupture from ever use to within 90 days from the index date, before (OR=1.10–1.37) and after (OR=1.10–1.31) adjustment. Patients prescribed anti-asthma drugs also showed an increased risk of rupture before (OR=1.12–1.79) and after (OR=1.09–1.48) the same adjustment. In Viborg vascular trial, anti-asthmatic medication use associated with increased risk of AAA before (OR=1.45) or after adjustment for smoking (OR=1.45) or other risk factors (OR=1.46). Conclusions—Recent active asthma increased risk of AAA and ruptured AAA. These findings document and furnish novel links between airway disease and AAA, 2 common diseases that share inflammatory aspects.