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自主神经系统在心脏炎症调节中的研究进展

[Research advances of autonomic nervous system in the regulation of cardiac inflammation].

作者信息

Feng Ye-Nan, Xiao Han, Zhang You-Yi

机构信息

Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.

出版信息

Sheng Li Xue Bao. 2019 Apr 25;71(2):225-234.

Abstract

The autonomic nervous system consists of the sympathetic nervous system and the parasympathetic nervous system. These two systems control the heart and work in a reciprocal fashion to modulate myocardial energy metabolism, heart rate as well as blood pressure. Multiple cardiac pathological conditions are accompanied by autonomic imbalance, characterized by sympathetic overactivation and parasympathetic inhibition. Studies have shown that overactive sympathetic nervous system leads to increased cardiac inflammatory reaction. Orchestrated inflammatory response serves to clear dead cardiac tissue and activate reparative process, whereas excessive inflammation may result in pathological cardiac remodeling. Since the discovery of the α7 nicotinic acetylcholine receptor (α7nAChR)-mediated cholinergic anti-inflammatory pathway (CAP), the protective effects of the parasympathetic nervous system in cardiac inflammation have attracted more attention recently. In this review, we summarized the role and underlying mechanisms of the sympathetic and parasympathetic nervous systems in cardiac inflammation, in order to provide new insight into cardiac inflammatory response in cardiovascular diseases.

摘要

自主神经系统由交感神经系统和副交感神经系统组成。这两个系统控制心脏,并以相互作用的方式调节心肌能量代谢、心率和血压。多种心脏病理状况伴有自主神经失衡,其特征为交感神经激活过度和副交感神经抑制。研究表明,交感神经系统过度活跃会导致心脏炎症反应增加。精心编排的炎症反应有助于清除坏死的心脏组织并激活修复过程,而过度炎症可能导致病理性心脏重塑。自从发现α7烟碱型乙酰胆碱受体(α7nAChR)介导的胆碱能抗炎通路(CAP)以来,副交感神经系统在心脏炎症中的保护作用最近受到了更多关注。在这篇综述中,我们总结了交感神经系统和副交感神经系统在心脏炎症中的作用及潜在机制,以便为心血管疾病中的心脏炎症反应提供新的见解。

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