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Updated: Jul 6, 2025

Location, Dissection, and Analysis of the Murine Stellate Ganglion
Published on: December 22, 2020
Mast cell stabilizer, an anti-allergic drug, reduces ventricular arrhythmia risk via modulation of neuroimmune
Yuhong Wang1, Zhihao Liu1, Wenjie Zhou1
1Department of Cardiology, Renmin Hospital of Wuhan University, Hubei Key Laboratory of Autonomic Nervous System Modulation, Cardiac Autonomic Nervous System Research Center of Wuhan University, Taikang Center for Life and Medical Sciences of Wuhan University, Hubei Key Laboratory of Cardiology, Cardiovascular Research Institute of Wuhan University, No. 238 Jiefang Road, Wuchang District, Wuhan City, 430060, Hubei Province, People's Republic of China.
Abstract:
Mast cells (MCs) are important intermediates between the nervous and immune systems. The cardiac autonomic nervous system (CANS) crucially modulates cardiac electrophysiology and arrhythmogenesis, but whether and how MC-CANS neuroimmune interaction influences arrhythmia remain unclear. Our clinical data showed a close relationship between serum levels of MC markers and CANS activity, and then we use mast cell stabilizers (MCSs) to alter this MC-CANS communication. MCSs, which are well-known anti-allergic agents, could reduce the risk of ventricular arrhythmia (VA) after myocardial infarction (MI). RNA-sequencing (RNA-seq) analysis to investigate the underlying mechanism by which MCSs could affect the left stellate ganglion (LSG), a key therapeutic target for modulating CANS, showed that the IL-6 and γ-aminobutyric acid (GABA)-ergic system may be involved in this process. Our findings demonstrated that MCSs reduce VA risk along with revealing the potential underlying antiarrhythmic mechanisms.
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