Abstract:
Aims: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. Methods and results: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. Conclusion: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.
journal_name
Cardiovasc Resjournal_title
Cardiovascular researchauthors
Cao N,Chen H,Bai Y,Yang X,Xu W,Hao W,Zhou Y,Chai J,Wu Y,Wang Z,Yin X,Wang L,Wang W,Liu H,Fu MLXdoi
10.1093/cvr/cvy105subject
Has Abstractpub_date
2018-09-01 00:00:00pages
1487-1498issue
11eissn
0008-6363issn
1755-3245pii
4993974journal_volume
114pub_type
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更新日期:2008-01-15 00:00:00
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doi:10.1016/j.cardiores.2005.07.010
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doi:10.1093/cvr/13.12.693
更新日期:1979-12-01 00:00:00
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doi:10.1093/cvr/cvt057
更新日期:2013-07-01 00:00:00
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doi:10.1016/j.cardiores.2006.02.020
更新日期:2006-05-01 00:00:00
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doi:10.1016/s0008-6363(99)00142-x
更新日期:1999-08-01 00:00:00
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doi:10.1016/j.cardiores.2005.02.004
更新日期:2005-06-01 00:00:00
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