P2X7 receptor inhibition prevents atrial fibrillation in rodent models of depression.
Tianxin YeYunping ZhouJinxiu YangFangcong YuZhuonan SongJiaran ShiLongbo WangZhou-Qing HuangBo YangXingxiang WangPublished in: Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology (2024)
LPS or CUS induces AF and promotes P2X7R-dependent activation of NLRP3 inflammasome, whereas pharmacological P2X7R inhibition or P2X7R genetic deficiency prevents atrial remodeling without interrupting normal atrial physiological functions. Our results point to P2X7R as an important factor in the pathology of AF in depression.
Keyphrases
- atrial fibrillation
- nlrp inflammasome
- catheter ablation
- left atrial
- oral anticoagulants
- depressive symptoms
- left atrial appendage
- direct oral anticoagulants
- sleep quality
- heart failure
- percutaneous coronary intervention
- mouse model
- inflammatory response
- genome wide
- gene expression
- coronary artery disease
- venous thromboembolism
- physical activity
- mitral valve
- replacement therapy
- smoking cessation