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RELM\u03b3 is part of a pore-forming protein family that defends the host against bacteria by perforating their membranes. In mice with acute infarcts, leukocyte-specific\n            <jats:italic toggle=\"yes\">Retnlg<\/jats:italic>\n            deletion reduced ventricular tachycardia. RELM\u03b3 elicited membrane defects that allowed cell exclusion dyes to enter the cardiomyocyte interior and also caused delayed afterdepolarizations and later cardiomyocyte death, both of which are strong arrhythmogenic triggers. Human resistin likewise attacked membranes of liposomes and mammalian cells. We describe how misdirected innate immune defense produces membrane leaks and ventricular arrhythmia.\n          <\/jats:p>","DOI":"10.1126\/science.adp7361","type":"journal-article","created":{"date-parts":[[2025,9,4]],"date-time":"2025-09-04T18:01:48Z","timestamp":1757008908000},"page":"1043-1048","update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":18,"title":["Resistin-like molecule \u03b3 attacks cardiomyocyte membranes and promotes ventricular tachycardia"],"prefix":"10.1126","volume":"389","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3355-9102","authenticated-orcid":true,"given":"Nina","family":"Kumowski","sequence":"first","affiliation":[{"name":"Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA."},{"name":"Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA."},{"name":"Center for Inflammation Imaging, Massachusetts 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