{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T17:56:24Z","timestamp":1791568584542,"version":"4.3.4"},"reference-count":34,"publisher":"National Academy of Sciences","issue":"7","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2012,2,14]]},"abstract":"<jats:p>\n                    Heart growth is tightly controlled so that the heart reaches a predetermined size. Fetal heart growth occurs through cardiomyocyte proliferation, whereas postnatal heart growth involves primarily physiological cardiomyocyte hypertrophy. The Hippo kinase cascade is an important regulator of organ growth. A major target of this kinase cascade is YAP1, a transcriptional coactivator that is inactivated by Hippo kinase activity. Here, we used both genetic gain and loss of\n                    <jats:italic>Yap1<\/jats:italic>\n                    function to investigate its role in regulating proliferative and physiologic hypertrophic heart growth. Fetal\n                    <jats:italic>Yap1<\/jats:italic>\n                    inactivation caused marked, lethal myocardial hypoplasia and decreased cardiomyocyte proliferation, whereas fetal activation of YAP1 stimulated cardiomyocyte proliferation. Enhanced proliferation was particularly dramatic in trabecular cardiomyocytes that normally exit from the cell cycle. Remarkably, YAP1 activation was sufficient to stimulate proliferation of postnatal cardiomyocytes, both in culture and in the intact heart. A dominant negative peptide that blocked YAP1 binding to TEAD transcription factors inhibited YAP1 proliferative activity, indicating that this activity requires YAP1\u2013TEAD interaction. Although Yap1 was a critical regulator of cardiomyocyte proliferation, it did not influence physiological hypertrophic growth of cardiomyocytes, because postnatal\n                    <jats:italic>Yap1<\/jats:italic>\n                    gain or loss of function did not significantly alter cardiomyocyte size. These studies demonstrate that\n                    <jats:italic>Yap1<\/jats:italic>\n                    is a crucial regulator of cardiomyocyte proliferation, cardiac morphogenesis, and myocardial trabeculation. Activation of\n                    <jats:italic>Yap1<\/jats:italic>\n                    in postnatal cardiomyocytes may be a useful strategy to stimulate cardiomyocyte expansion in therapeutic myocardial regeneration.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1116136109","type":"journal-article","created":{"date-parts":[[2012,1,31]],"date-time":"2012-01-31T01:24:54Z","timestamp":1327973094000},"page":"2394-2399","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":561,"title":["YAP1, the nuclear target of Hippo signaling, stimulates heart growth through cardiomyocyte proliferation but not hypertrophy"],"prefix":"10.1073","volume":"109","author":[{"given":"Alexander","family":"von Gise","sequence":"first","affiliation":[{"name":"Department of Cardiology and"},{"name":"Department of Neonatology, Charit\u00e9 University Medical Center, 10117 Berlin, Germany;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhiqiang","family":"Lin","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karin","family":"Schlegelmilch","sequence":"additional","affiliation":[{"name":"Stem Cell Program, Children's Hospital Boston, Boston, MA 02115;"},{"name":"Institute for Chemistry\/Biochemistry, Freie Universit\u00e4t Berlin, 14195 Berlin, Germany;"},{"name":"Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138;"},{"name":"Harvard Stem Cell Institute, Cambridge, MA 02138;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leah B.","family":"Honor","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gina M.","family":"Pan","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica N.","family":"Buck","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qing","family":"Ma","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takahiro","family":"Ishiwata","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Internal Medicine, University of Utah, Salt Lake City, UT 84132; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bin","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"},{"name":"Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fernando D.","family":"Camargo","sequence":"additional","affiliation":[{"name":"Stem Cell Program, Children's Hospital Boston, Boston, MA 02115;"},{"name":"Department of Stem Cell and Regenerative Biology, Harvard University, Cambridge, MA 02138;"},{"name":"Harvard Stem Cell Institute, Cambridge, MA 02138;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William T.","family":"Pu","sequence":"additional","affiliation":[{"name":"Department of Cardiology and"},{"name":"Harvard Stem Cell Institute, Cambridge, MA 02138;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2012,1,30]]},"reference":[{"key":"e_1_3_4_1_2","doi-asserted-by":"crossref","first-page":"857","DOI":"10.1161\/01.RES.0000100389.57520.1A","article-title":"Developmental changes in ventricular diastolic function correlate with changes in ventricular myoarchitecture in normal mouse embryos","volume":"93","author":"Ishiwata T","year":"2003","unstructured":"T Ishiwata, M Nakazawa, WT Pu, SG Tevosian, S Izumo, Developmental changes in ventricular diastolic function correlate with changes in ventricular myoarchitecture in normal mouse embryos. 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Curr Opin Cell Biol 20, 638\u2013646 (2008).","journal-title":"Curr Opin Cell Biol"},{"key":"e_1_3_4_4_2","doi-asserted-by":"crossref","first-page":"457","DOI":"10.1016\/S0092-8674(03)00557-9","article-title":"The Drosophila Mst ortholog, hippo, restricts growth and cell proliferation and promotes apoptosis","volume":"114","author":"Harvey KF","year":"2003","unstructured":"KF Harvey, CM Pfleger, IK Hariharan, The Drosophila Mst ortholog, hippo, restricts growth and cell proliferation and promotes apoptosis. Cell 114, 457\u2013467 (2003).","journal-title":"Cell"},{"key":"e_1_3_4_5_2","doi-asserted-by":"crossref","first-page":"675","DOI":"10.1016\/j.cell.2004.12.036","article-title":"Control of cell proliferation and apoptosis by mob as tumor suppressor, mats","volume":"120","author":"Lai ZC","year":"2005","unstructured":"ZC Lai, et al., Control of cell proliferation and apoptosis by mob as tumor suppressor, mats. Cell 120, 675\u2013685 (2005).","journal-title":"Cell"},{"key":"e_1_3_4_6_2","doi-asserted-by":"crossref","first-page":"921","DOI":"10.1038\/ncb1051","article-title":"The Salvador partner Hippo promotes apoptosis and cell-cycle exit in Drosophila","volume":"5","author":"Pantalacci S","year":"2003","unstructured":"S Pantalacci, N Tapon, P L\u00e9opold, The Salvador partner Hippo promotes apoptosis and cell-cycle exit in Drosophila. Nat Cell Biol 5, 921\u2013927 (2003).","journal-title":"Nat Cell Biol"},{"key":"e_1_3_4_7_2","doi-asserted-by":"crossref","first-page":"445","DOI":"10.1016\/S0092-8674(03)00549-X","article-title":"hippo encodes a Ste-20 family protein kinase that restricts cell proliferation and promotes apoptosis in conjunction with salvador and warts","volume":"114","author":"Wu S","year":"2003","unstructured":"S Wu, J Huang, J Dong, D Pan, hippo encodes a Ste-20 family protein kinase that restricts cell proliferation and promotes apoptosis in conjunction with salvador and warts. 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