{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T20:04:39Z","timestamp":1792785879772,"version":"4.5.0"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"36","license":[{"start":{"date-parts":[[2026,5,18]],"date-time":"2026-05-18T00:00:00Z","timestamp":1779062400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82088101"],"award-info":[{"award-number":["82088101"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82321005"],"award-info":[{"award-number":["82321005"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82222008"],"award-info":[{"award-number":["82222008"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82470330"],"award-info":[{"award-number":["82470330"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Fundamental and Interdisciplinary Disciplines Breakthrough Plan of the Ministry of Education of China","award":["JYB2025XDXM601"],"award-info":[{"award-number":["JYB2025XDXM601"]}],"id":[{"id":"https:\/\/ror.org\/03m01yf64","id-type":"ROR","asserted-by":"crossref"}]},{"name":"Key Research Center Construction Project of Shanghai","award":["2022ZZ01008"],"award-info":[{"award-number":["2022ZZ01008"]}]},{"DOI":"10.13039\/501100012232","name":"National Key Clinical Specialty","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100012232","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,9,22]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background and Aims<\/jats:title>\n                    <jats:p>Fatal ventricular tachyarrhythmias (FVTs) are a major cause of sudden cardiac death globally. Despite their clinical importance, current antiarrhythmic therapies remain constrained by limited efficacy and proarrhythmic risks. Although endogenous cardiac cholinergic signalling contributes to electrophysiological regulation, the therapeutic potential of targeting ventricular \u03b14\u03b22 nicotinic acetylcholine receptors (nAChRs), a pivotal component of this system, for FVT treatment remains to be elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A pharmacological screen identified positive allosteric modulators (PAMs) of \u03b14\u03b22 nAChRs as possessing antiarrhythmic properties. Through structure-based design, salvage-1 was developed and its efficacy and safety profile were evaluated in rodent, porcine, and human ex vivo heart models of FVTs. The underlying mechanism was investigated using patch-clamp electrophysiology, high-resolution optical mapping, and molecular dynamics simulations.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Pharmacological screening validated the potentiation of \u03b14\u03b22 nAChRs as a promising antiarrhythmic strategy. Structure-guided development yielded salvage-1, a PAM that selectively engages Phe312 and Phe316 on the \u03b14 subunit to stabilize the receptor in an open-channel state. Across rodent, porcine, and human ex vivo heart models of FVTs, salvage-1 consistently prevented arrhythmogenesis and rapidly restored sinus rhythm. Mechanistically, salvage-1 enhanced acetylcholine-gated currents, selectively improved conduction velocity in injured myocardium, and suppressed re-entry, without compromising electrophysiology in healthy tissue.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>This study identifies ventricular \u03b14\u03b22 nAChRs as a druggable target for FVTs and introduces salvage-1 as a first-in-class therapeutic candidate, thereby establishing a new direction for the pharmacological therapy of cardiac arrhythmias.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eurheartj\/ehag293","type":"journal-article","created":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T11:44:14Z","timestamp":1775648654000},"page":"5094-5108","source":"Crossref","is-referenced-by-count":2,"title":["Cardiac \u03b14\u03b22 nicotinic receptors as a therapeutic target for fatal ventricular 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