GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Oxford University Press (OUP)  (2)
  • Wang, Jing  (2)
  • English  (2)
Material
Publisher
  • Oxford University Press (OUP)  (2)
Language
  • English  (2)
Years
Subjects(RVK)
  • 1
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 54, No. 6 ( 2008-06-01), p. 1046-1052
    Abstract: Background: Several studies have suggested an association between antibody to human heat shock protein 60 (anti-Hsp60) and coronary atherosclerosis, but the results have been inconsistent. The aim of this study was to investigate the association between anti-Hsp60 and coronary heart disease (CHD) and to determine whether anti-Hsp60, hypertension, and diabetes have joint effects on CHD risk. Methods: We measured the concentrations of anti-Hsp60 in 1003 CHD patients and 1003 age- and sex-matched control subjects without CHD events. Results: Concentrations of anti-Hsp60 were significantly higher in CHD patients than in controls. Increasing concentrations of anti-Hsp60 were significantly associated with higher risk of CHD (P for trend & lt;0.0001) and with increasing severity of CHD as assessed by number of diseased vessels detected with angiography [odds ratio (OR) 3.67, 95% CI 1.56–8.64, P = 0.003] after multivariate adjustment for traditional CHD risk factors. There were strong joint effects of high concentrations of anti-Hsp60 and hypertension (OR 5.17, 95% CI 3.95–6.75, P & lt; 0.0001) and diabetes (OR 6.49, 95% CI 4.52–9.33, P & lt; 0.0001) on CHD risk; simultaneous occurrence of high anti-Hsp60 concentrations, hypertension, and diabetes conferred a dramatically higher risk of CHD (OR 20.99, 95% CI 12.50–35.24, P & lt; 0.0001) in multivariate analyses. Conclusions: Anti-Hsp60 is independently associated with CHD risk, and a combination of high anti-Hsp60, hypertension, and diabetes is particularly detrimental for CHD risk.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2008
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2022
    In:  Cardiovascular Research Vol. 118, No. 14 ( 2022-11-10), p. 2985-2999
    In: Cardiovascular Research, Oxford University Press (OUP), Vol. 118, No. 14 ( 2022-11-10), p. 2985-2999
    Abstract: Hypertension is the major cause of cardiovascular diseases and global mortality. Immunoglobulin E (IgE), which plays crucial roles in allergic diseases, has been implicated in the pathogenesis of vascular and cardiac remodelling via its receptor (FcεR1). In this study, we aimed to reveal the role of IgE and FcεR1 in hypertension. Methods and results Herein, we reported that IgE levels were significantly increased in hypertensive patients as well as in hypertensive mice induced by angiotensin II (Ang II). Ang II-induced vascular remodelling and hypertension were significantly alleviated in FcεR1 genetic knockout mice or in mice treated with anti-IgE monoclonal antibody. Similarly, treatment with omalizumab (a clinical IgE antagonist) also markedly inhibited Ang II-induced hypertension. Furthermore, the cellular contribution of IgE–FcεR1 in hypertension was evaluated in mice with FcεR1 conditional knockout in mast cell (MC), smooth muscle cell (SMC), or endothelial cell (EC). Our data revealed that IgE-mediated hypertension is largely dependent on FcεR1 in MCs but not SMCs and ECs. Finally, RNA-seq and signalling pathway analyses of mouse bone marrow-derived MCs suggested that interleukin 6 (IL-6) is one of critical mediators in IgE-mediated hypertension. IL-6 derived from IgE-stimulated MCs promoted reactive oxygen species production and decreased the levels of phosphorylated endothelial nitric oxide synthase in ECs, leading to endothelial dysfunction. Conclusion Our findings reveal that IgE contributes to the pathogenesis of hypertension, at least partially through activating the IgE–FcεR1 signalling in MCs. Thus, IgE may represent a new therapeutic target for IgE-mediated hypertension.
    Type of Medium: Online Resource
    ISSN: 0008-6363 , 1755-3245
    RVK:
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2022
    detail.hit.zdb_id: 1499917-1
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...