CCRR regulate MYZAP-PKP2-Nav1.5 signaling pathway in atrial fibrillation following myocardial infarction

Atrial fibrillation (AF) is the most common sustained arrhythmia which brings a heavy burden to the lives and health of patients worldwide. Our earlier research documented cardiac conduction regulatory RNA (CCRR) as an antiarrhythmic lncRNA in heart failure. Here, we report that CCRR was decreased in atrial tissue after MI, MYZAP, and Nav1.5 were increased in the atrium in cardiac-specific transgenic CCRR overexpression mice. Overexpression of CCRR carried by AAV-9 reversed the incidence and duration of AF and atrial conduction velocity in MI mice. MYZAP overexpression reversed the decreasing levels of PKP2, Nav1.5, and AF incidence after MI in addition to downregulating the expression levels of TLR2, TLR4, and inflammation-related factors following MI. Our work revealed that CCRR can improve the occurrence and development of AF after MI through the MYZAP-PKP2 pathway and inhibit Nav1.5 and TLR signaling pathways associated with inflammation, thus serving as a therapeutic target for AF.

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Publication Details

Journal
iScience
Published
2024-10-04
DOI
https://doi.org/10.1016/j.isci.2024.111102
Citations
3
Primary Topic
Cardiac electrophysiology and arrhythmias
Type
article
Field-Weighted Citation Impact
1.21

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article

CCRR regulate MYZAP-PKP2-Nav1.5 signaling pathway in atrial fibrillation following myocardial infarction

Siyun Li, Lihua Sun, Hua Yang, Guangze Wang et al.
3 citations
iScience
Cardiac electrophysiology and arrhythmias
1.21
article

CCRR regulate MYZAP-PKP2-Nav1.5 signaling pathway in atrial fibrillation following myocardial infarction

Siyun Li, Lihua Sun, Hua Yang, Guangze Wang, Xiao Hu, Huishan Luo, Shengjie Wang, Lina Xuan, Qingqing Zhang, Hailong Zhang, Baofeng Yang, Jianjun Guo, Feihan Sun, Shijia Cui, Xingmei Yang
article en
3 citations

Abstract

Atrial fibrillation (AF) is the most common sustained arrhythmia which brings a heavy burden to the lives and health of patients worldwide. Our earlier research documented cardiac conduction regulatory RNA (CCRR) as an antiarrhythmic lncRNA in heart failure. Here, we report that CCRR was decreased in atrial tissue after MI, MYZAP, and Nav1.5 were increased in the atrium in cardiac-specific transgenic CCRR overexpression mice. Overexpression of CCRR carried by AAV-9 reversed the incidence and duration of AF and atrial conduction velocity in MI mice. MYZAP overexpression reversed the decreasing levels of PKP2, Nav1.5, and AF incidence after MI in addition to downregulating the expression levels of TLR2, TLR4, and inflammation-related factors following MI. Our work revealed that CCRR can improve the occurrence and development of AF after MI through the MYZAP-PKP2 pathway and inhibit Nav1.5 and TLR signaling pathways associated with inflammation, thus serving as a therapeutic target for AF.

iScienceVol. 27(11)
Harbin Medical University (CN), Chinese Academy of Medical Sciences & Peking Union Medical College (CN), Heilongjiang Academy of Sciences (CN)
Harbin Medical University, Innovative Research Group Project of the National Natural Science Foundation of China, National Natural Science Foundation of China, Natural Science Foundation of Heilongjiang Province
Zero hunger
Openalex Percentile: Top 18%
Cardiac electrophysiology and arrhythmias
1.21
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