{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T18:16:38Z","timestamp":1790705798480,"version":"4.1.0"},"reference-count":70,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T00:00:00Z","timestamp":1771113600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T00:00:00Z","timestamp":1771113600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100000274","name":"British Heart Foundation","doi-asserted-by":"publisher","award":["SP\/F\/22\/150027"],"award-info":[{"award-number":["SP\/F\/22\/150027"]}],"id":[{"id":"10.13039\/501100000274","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000268","name":"Biotechnology and Biological Sciences Research Council","doi-asserted-by":"publisher","award":["BB\/Y006488\/1"],"award-info":[{"award-number":["BB\/Y006488\/1"]}],"id":[{"id":"10.13039\/501100000268","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Sudden cardiac death in young individuals with structurally normal hearts represents a critical unresolved clinical challenge and typically occurs in patients with inherited arrhythmia syndromes due to cardiac channelopathies. Catecholaminergic polymorphic ventricular tachycardia (CPVT) can cause fatal arrhythmias triggered by adrenergic stimulation. Therapeutic interventions primarily target cardiac myocytes (CMs) despite robust clinical evidence demonstrating the life\u2010saving efficacy of cardiac sympathetic denervation. To understand this therapeutic paradox, we developed human induced pluripotent stem cell (hiPSC)\u2010derived CMs and sympathetic neurons (SNs) from healthy individuals and CPVT patients to investigate neurocardiac interactions using two\u2010 and three\u2010dimensional microtissue models. We tested the hypothesis that CPVT is also a disease of the autonomic nervous system and observed that CPVT hiPSC\u2010derived SNs had enhanced calcium transients, elevated cyclic adenosine monophosphate levels, and hyperexcitability, similar to diseased cardiomyocytes. Critically, co\u2010culturing diseased neurons with healthy CMs induced arrhythmogenic activity, establishing that neuronal dysfunction directly triggers cardiac arrhythmias. Multielectrode array recordings, optical mapping and single\u2010cell RNA sequencing revealed dysregulated neurotransmitter pathways and identified druggable molecular targets within SNs. These findings may explain why surgically interrupting sympathetic nerves helps CPVT patients and identify the nervous system as a therapeutic target. They further suggest that CPVT is more than a disease of the CM and should be re\u2010defined as a neuro\u2010cardiac disorder that paves the way for neuromodulation therapy.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp70392-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>Sympathetic nerve overactivity is pro\u2010arrhythmic and a key contributor to ventricular tachycardia and sudden cardiac death in patients with cardiac channelopathies.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Catecholaminergic polymorphic ventricular tachycardia (CPVT) sympathetic neurons (SNs) exhibit enhanced calcium transients, elevated cAMP levels, and hyperexcitability that directly trigger arrhythmias in healthy cardiomyocytes.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Novel human induced pluripotent stem cell\u2010derived cardiac\u2010neural microtissue models reveal CPVT is also a neurological disorder involving dysfunctional neurocardiac interactions.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Single\u2010cell RNA sequencing identifies dysregulated neurotransmitter pathways in SNs, providing new therapeutic targets for neuromodulation therapy.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp290024","type":"journal-article","created":{"date-parts":[[2026,2,15]],"date-time":"2026-02-15T16:57:00Z","timestamp":1771174620000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Human\u2010derived cardiac\u2010neural microtissues reveal catecholaminergic polymorphic ventricular tachycardia is also a disease of the sympathetic neuron"],"prefix":"10.1113","author":[{"given":"Ni","family":"Li","sequence":"first","affiliation":[{"name":"Burdon Sanderson Cardiac Science Centre and BHF Centre of Research Excellence, Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"},{"name":"Sun Yat\u2010Sen Memorial Hospital Sun Yat\u2010Sen University  Guangzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chenchen","family":"Zhang","sequence":"additional","affiliation":[{"name":"Institute of Electrophysiology Henan Academy of Innovations in Medical Science  Zhengzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mengying","family":"Xu","sequence":"additional","affiliation":[{"name":"Institute of Electrophysiology Henan Academy of Innovations in Medical Science  Zhengzhou China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YoonYoung","family":"Choi","sequence":"additional","affiliation":[{"name":"Burdon Sanderson Cardiac Science Centre and BHF Centre of Research Excellence, Department of Physiology, Anatomy and Genetics University of Oxford  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Davi","family":"Sidarta\u2010Oliveira","sequence":"additional","affiliation":[{"name":"Burdon Sanderson Cardiac Science Centre and BHF Centre of 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