{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T18:46:10Z","timestamp":1791830770135,"version":"4.3.4"},"reference-count":70,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"15","license":[{"start":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T00:00:00Z","timestamp":1791849600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2026,10,13]]},"abstract":"<jats:sec>\n                    <jats:title>BACKGROUND:<\/jats:title>\n                    <jats:p>Myocardial infarction can cause a massive loss of functional cardiomyocytes, yet effective strategies to stimulate cardiac regeneration remain lacking. A key barrier to adult cardiomyocyte proliferation appears to be cytokinesis inhibition. This study aimed to determine whether combining proliferation stimulators with the removal of cytokinesis-inhibitory constraints could unlock regenerative potential after myocardial infarction.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS:<\/jats:title>\n                    <jats:p>\n                      Transcriptomic profile from 5 regeneration models, including\n                      <jats:italic toggle=\"yes\">Aurkb<\/jats:italic>\n                      -tdTomato cytokinesis reporter mice and\n                      <jats:italic toggle=\"yes\">Myh6<\/jats:italic>\n                      -MerCreMer;mosaic analysis with double markers (MADM), and cross-species comparative analysis were used to explore the regulatory networks for cardiomyocyte proliferation. MADM mice were used to evaluate cardiac regeneration by quantifying after cytokinesis new cardiomyocytes and clonal clusters.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS:<\/jats:title>\n                    <jats:p>\n                      Integrative multimodel analysis revealed a dual regulatory control system for cardiomyocyte proliferation, along with key associated genes and transcriptional regulators.\n                      <jats:italic toggle=\"yes\">Nfyb<\/jats:italic>\n                      was identified as an activator and\n                      <jats:italic toggle=\"yes\">Nr3c1<\/jats:italic>\n                      as a repressor of cardiomyocyte proliferation.\n                      <jats:italic toggle=\"yes\">Nfyb<\/jats:italic>\n                      overexpression enhanced cardiomyocyte proliferation and post\u2013myocardial infarction cardiac repair through propelling cell-cycle gene transcription.\n                      <jats:italic toggle=\"yes\">Nr3c1<\/jats:italic>\n                      inhibition promoted cardiomyocyte proliferation, improved cardiac function, and reduced infarct size. A spatiotemporally controlled adeno-associated virus 9 system combining drug-inducible\n                      <jats:italic toggle=\"yes\">Nfyb<\/jats:italic>\n                      overexpression and CRISPR\/enOsCas12f1\u2013mediated\n                      <jats:italic toggle=\"yes\">Nr3c1<\/jats:italic>\n                      deletion efficiently induces cardiomyocyte proliferation. Clonal analysis using MADM mice showed that the dual intervention synergistically increased new cardiomyocyte formation (28% clustered, &gt;28-fold versus control). The enhanced regenerative effect of the dual intervention was demonstrated in post\u2013myocardial infarction mice and human engineered heart tissues.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>CONCLUSIONS:<\/jats:title>\n                    <jats:p>\n                      This work documents a dual-control paradigm of cardiomyocyte proliferation and establishes\n                      <jats:italic toggle=\"yes\">Nfyb<\/jats:italic>\n                      \/\n                      <jats:italic toggle=\"yes\">Nr3c1<\/jats:italic>\n                      cointervention as a putative new therapy to induce and control cardiac regeneration after injury.\n                    <\/jats:p>\n                  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Southwest Hospital of Army Medical University (Third Military Medical University), China (B.L., W.L., Z.G., J.Z., L.M., J.S., Y.L., C.C., J.Z., S.T., W.E.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wujian","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Xinqiao Hospital (B.L., W.L., Z.G., J.Z., Y.X., J.S., Y.L., J.Z., Z.L., S.T., W.E.W.), Army Medical University (Third Military Medical University), Chongqing, China."},{"name":"Department of Geriatrics, Chongqing Key Laboratory of Aging and Regeneration Medicine, Southwest Hospital of Army Medical University (Third Military Medical University), China (B.L., W.L., Z.G., J.Z., L.M., J.S., Y.L., C.C., J.Z., S.T., W.E.W.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ziyan","family":"Ge","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Xinqiao Hospital (B.L., W.L., Z.G., J.Z., Y.X., J.S., Y.L., J.Z., Z.L., S.T., W.E.W.), Army 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