{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T22:17:15Z","timestamp":1792621035269,"version":"4.5.0"},"reference-count":68,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2016,4,15]]},"abstract":"<jats:sec>\n                    <jats:title>\n                      <jats:underline>Rationale:<\/jats:underline>\n                    <\/jats:title>\n                    <jats:p>Cardiac myocyte\u2013specific deletion of either glycogen synthase kinase (GSK)-3\u03b1 and GSK-3\u03b2 leads to cardiac protection after myocardial infarction, suggesting that deletion of both isoforms may provide synergistic protection. This is an important consideration because of the fact that all GSK-3\u2013targeted drugs, including the drugs already in clinical trial target both isoforms of GSK-3, and none are isoform specific.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>\n                      <jats:underline>Objective:<\/jats:underline>\n                    <\/jats:title>\n                    <jats:p>To identify the consequences of combined deletion of cardiac myocyte GSK-3\u03b1 and GSK-3\u03b2 in heart function.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>\n                      <jats:underline>Methods and Results:<\/jats:underline>\n                    <\/jats:title>\n                    <jats:p>We generated tamoxifen-inducible cardiac myocyte\u2013specific mice lacking both GSK-3 isoforms (double knockout). We unexpectedly found that cardiac myocyte GSK-3 is essential for cardiac homeostasis and overall survival. Serial echocardiographic analysis reveals that within 2 weeks of tamoxifen treatment, double-knockout hearts leads to excessive dilatative remodeling and ventricular dysfunction. Further experimentation with isolated adult cardiac myocytes and fibroblasts from double-knockout implicated cardiac myocytes intrinsic factors responsible for observed phenotype. Mechanistically, loss of GSK-3 in adult cardiac myocytes resulted in induction of mitotic catastrophe, a previously unreported event in cardiac myocytes. Double-knockout cardiac myocytes showed cell cycle progression resulting in increased DNA content and multinucleation. However, increased cell cycle activity was rivaled by marked activation of DNA damage, cell cycle checkpoint activation, and mitotic catastrophe\u2013induced apoptotic cell death. Importantly, mitotic catastrophe was also confirmed in isolated adult cardiac myocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>\n                      <jats:underline>Conclusions:<\/jats:underline>\n                    <\/jats:title>\n                    <jats:p>Together, our findings suggest that cardiac myocyte GSK-3 is required to maintain normal cardiac homeostasis, and its loss is incompatible with life because of cell cycle dysregulation that ultimately results in a severe fatal dilated cardiomyopathy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circresaha.116.308544","type":"journal-article","created":{"date-parts":[[2016,3,14]],"date-time":"2016-03-14T23:25:05Z","timestamp":1457997905000},"page":"1208-1222","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":106,"title":["Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy"],"prefix":"10.1161","volume":"118","author":[{"given":"Jibin","family":"Zhou","sequence":"first","affiliation":[{"name":"From the Division of Cardiovascular Medicine (F.A., V.K.V., Y.G., H.L., T.F.) and Department of Pharmacology (S.P., Y.G.), Vanderbilt University Medical Center, Nashville, TN; Department of Medicine, Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA (J.Z., N.E.H., S.R., J.S., A.Y., S.S., E.G., W.K., M.M., R.K.); and Department of Medical Biophysics, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada (J.R.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Firdos","family":"Ahmad","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Medicine (F.A., V.K.V., Y.G., H.L., T.F.) and Department of Pharmacology (S.P., Y.G.), Vanderbilt University Medical Center, Nashville, TN; Department of Medicine, Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA (J.Z., N.E.H., S.R., J.S., A.Y., S.S., E.G., W.K., M.M., R.K.); and Department of Medical Biophysics, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada (J.R.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shan","family":"Parikh","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Medicine (F.A., V.K.V., Y.G., H.L., T.F.) and Department of Pharmacology (S.P., Y.G.), Vanderbilt University Medical Center, Nashville, TN; Department of Medicine, Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA (J.Z., N.E.H., S.R., J.S., A.Y., S.S., E.G., W.K., M.M., R.K.); and Department of Medical Biophysics, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada (J.R.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nichole E.","family":"Hoffman","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Medicine (F.A., V.K.V., Y.G., H.L., T.F.) and Department of Pharmacology (S.P., Y.G.), Vanderbilt University Medical Center, Nashville, TN; Department of Medicine, Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA (J.Z., N.E.H., S.R., J.S., A.Y., S.S., E.G., W.K., M.M., R.K.); and Department of Medical Biophysics, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada (J.R.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sudarsan","family":"Rajan","sequence":"additional","affiliation":[{"name":"From the Division of Cardiovascular Medicine (F.A., V.K.V., Y.G., H.L., T.F.) and Department of Pharmacology (S.P., Y.G.), Vanderbilt University Medical Center, Nashville, TN; 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