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This results in diminished cardiac contractility and impaired cardiac function. In cardiac tissue, the underlying molecular mechanisms responsible for RyR2\u2010independent Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010leak are poorly understood. Mitsugumin 23 (MG23) is an intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010conducting ion channel located on endoplasmic\/sarcoplasmic reticulum (ER\/SR) and nuclear membranes. We propose that MG23 contributes to regulation of intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010homeostasis, and that altered MG23 function may drive progression of cardiac dysfunction. The aim of this research was to investigate the role of MG23 in SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010leak, and whether knockout of\n                    <jats:italic>Mg23<\/jats:italic>\n                    protects the heart against pressure\u2010overload induced left ventricular hypertrophy. Cardiac pressure\u2010overload was induced in wild type (WT) and\n                    <jats:italic>Mg23<\/jats:italic>\n                    \u2010knockout (KO) mice through subcutaneous Angiotensin II (AngII, 1.1\u2009mg\/kg\/day) infusion via osmotic pump. After 10\u2010day infusion, in\u00a0vivo pressure\u2010volume dynamics were measured by insertion of a pressure\u2010volume catheter into the left ventricle. MG23 protein expression was assessed through Western blot analysis. Ventricular fibrosis and cardiomyocyte size were measured using histological and immunofluorescence approaches. Cardiomyocytes were isolated from WT and\n                    <jats:italic>Mg23<\/jats:italic>\n                    \u2010KO hearts and intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010dynamics assessed through live cell imaging using the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    indicator Fluo\u20104. AngII\u2010induced cardiac pressure\u2010overload increased expression of MG23 in WT mouse hearts. Knockout of\n                    <jats:italic>Mg23<\/jats:italic>\n                    protected hearts against AngII\u2010induced cardiac hypertrophy. Compared to WT animals, AngII treated\n                    <jats:italic>Mg23<\/jats:italic>\n                    \u2010KO mice displayed a significant reduction in left ventricular fibrosis and displayed normal cardiac functioning. Overexpression of MG23 in the ventricular cell line H9C2, resulted in reduced SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    store levels. In\n                    <jats:italic>Mg23\u2010<\/jats:italic>\n                    KO hearts, no alteration in expression of key Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010handling proteins was identified, but cardiomyocytes displayed altered Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010spark profiles consistent with a role for MG23 in SR Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010leak. MG23 plays a key role in driving Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010dysregulation observed in the early pathological stages of pressure\u2010overload induced heart failure.\n                  <\/jats:p>","DOI":"10.1096\/fj.202500832r","type":"journal-article","created":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T13:58:45Z","timestamp":1769090325000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Knockout of the Intracellular Calcium Conducting Ion Channel Mitsugumin 23 (\n                    <scp>MG23<\/scp>\n                    ) Protects Against Pressure Overload Induced Left Ventricular Hypertrophy and Cardiac Dysfunction"],"prefix":"10.1096","volume":"40","author":[{"given":"Amy M.","family":"Dorward","sequence":"first","affiliation":[{"name":"School of Medicine University of St Andrews  St Andrews 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