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β2-adrenergic receptor autoantibodies alleviated myocardial damage induced by β1-adrenergic receptor autoantibodies in heart failure.

Journal article
Authors Ning Cao
Hao Chen
Yan Bai
Xiaochun Yang
Wenli Xu
Weiwei Hao
Yi Zhou
Jiayin Chai
Ye Wu
Zhaojia Wang
Xiaochen Yin
Li Wang
Wen Wang
Huirong Liu
Michael Fu
Published in Cardiovascular research
Volume 114
Issue 11
Pages 1487-1498
ISSN 1755-3245
Publication year 2018
Published at
Pages 1487-1498
Language en
Links dx.doi.org/10.1093/cvr/cvy105
www.ncbi.nlm.nih.gov/entrez/query.f...
Subject categories Clinical Medicine

Abstract

β1-adrenergic receptor autoantibodies (β1-AAs) and β2-adrenergic receptor autoantibodies (β2-AAs) are present in patients with heart failure (HF); however, their interrelationship with cardiac structure and function remains unknown. This study explored the effects of the imbalance between β1-AAs and β2-AAs on cardiac structure and its underlying mechanisms in HF.Patients with left systolic HF who suffered from coronary heart disease (65.9%) or dilated cardiomyopathy (34.1%) were divided into New York Heart Association Classes I-II (n = 51) and Classes III-IV (n = 37) and compared with healthy volunteers as controls (n = 41). Total immunoglobulin G from HF patient serum comprising β1-AAs and/or β2-AAs were determined and purified for in vitro studies from neonatal rat cardiomyocytes (NRCMs). In addition, HF was induced by doxorubicin in mice. We observed that the increased ratio of β1-AAs/β2-AAs was associated with worsening HF in patients. Moreover, β2-AAs from patients with HF suppressed the hyper-shrinking and apoptosis of NRCMS induced by β1-AAs from some patients. Finally, β2-AAs alleviated both myocardial damage and β1-AAs production induced by doxorubicin in mice.β2-AAs were capable of antagonizing the effects imposed by β1-AAs both in vitro and in vivo. The imbalance of β1-AAs and β2-AAs in patients with HF is a mechanism underlying HF progression, and the increasing ratio of β1-AAs/β2-AAs should be considered a clinical assessment factor for the deterioration of cardiac function in patients with HF.

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