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The superior cervical ganglion (SCG) is an extracardiac sympathetic ganglion which regulates cardiac autonomic tone. We aimed to investigate the characteristics and functional significance of SCG on neuro\u2010cardiac communication post\u2010MI.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Constructed MI rat model by left anterior descending coronary artery ligation, and electrophysiological, SCG sympathetic nerve activity testing, echocardiography and histology study were performed. The proteins and gene expression were detected using RNA\u2010seq, spatial transcriptomics, quantitative PCR, and western blotting.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>The SCG neuronal remodeling was recognized by significant increase in adrenergic tyrosine hydroxylase (TH) (+) neurons and decrease in neuronal size. Top differentially expressed genes enriched in pro\u2010inflammatory profile and nerve regulatory factor in left SCG (LSCG) post\u2010MI. Interleukin (IL)\u20101\u03b2 and IL\u20106 increased significantly at Day 3, ahead of nerve growth factor (NGF) which peaked at Day 7 post\u2010MI. Spatial transcriptomics further identified the relativity of TH enrichment with macrophages and cytokines. Therapeutic LSCG\u2010ectomy successfully triggered cardiac denervation and improved VA vulnerability. Eventually, cardiac denervation attenuated macrophage\/mast cell infiltration at para\u2010infarct regions, thus improved cardiac dysfunction. Mechanism study revealed that genetic knockdown of NGF receptor trkA in LSCG reversed sympathetic remodeling and cardiac inflammation, which may be partially mediated by substance P and calcitonin gene\u2010related peptide (CGRP).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Extracardiac sympathetic LSCG remodeling participated in arrhythmogenesis and cardiac inflammation\/function post\u2010MI. NGF bridged neuro\u2010immune crosstalk between pro\u2010inflammatory shifting and sympathetic overdrive. Targeting LSCG modification facilitated cardiac protection and prevented VAs post\u2010MI.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/apha.14279","type":"journal-article","created":{"date-parts":[[2025,1,13]],"date-time":"2025-01-13T06:17:44Z","timestamp":1736749064000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Left superior cervical ganglia lymph node mimicry and its role in rat ventricular arrhythmias following myocardial infarction"],"prefix":"10.1111","volume":"241","author":[{"given":"Qingxia","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Cardiology, Cheeloo College of Medicine, Shandong Provincial Qianfoshan Hospital Shandong University  Jinan China"},{"name":"Department of Critical Care Medicine Yantai Yuhuangding Hospital Affiliated with Medical Colledge of Qingdao University  Yantai 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