{"title":"Ctnna3缺乏通过增强新生小鼠心肌细胞增殖促进心脏再生。","authors":"Sha Zou, Wuhou Dai, Wufan Tao, Jifen Li, Zeyi Cheng, Hongyan Wang","doi":"10.31083/FBL39676","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Heart regeneration requires renewal of lost cardiomyocytes. However, the mammalian heart loses its proliferative capacity soon after birth, and the molecular signaling underlying the loss of cardiac proliferation postnatally is not fully understood.</p><p><strong>Purpose: </strong>This study aimed to investigate the role of Catenin alpha 3 (<i>Ctnna3</i>), coding for alpha T catenin (αT-catenin) protein in regulating cardiomyocyte proliferation and heart regeneration during the neonatal period.</p><p><strong>Methods: </strong>Here we report that ablation of <i>Ctnna3</i> and highly expressed in hearts, accelerated heart regeneration following heart apex resection in neonatal mice.</p><p><strong>Results: </strong>Our results show that <i>Ctnna3</i> deficiency enhances cardiomyocyte proliferation in hearts from postnatal day 7 (P7) mice by upregulating Yes-associated protein (Yap) expression.</p><p><strong>Conclusion: </strong>Our study demonstrates that <i>Ctnna3</i> deficiency is sufficient to promote heart regeneration and cardiomyocyte proliferation in neonatal mice and indicates that functional interference of α-catenins might help to stimulate myocardial regeneration after injury.</p>","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"30 7","pages":"39676"},"PeriodicalIF":3.1000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"<i>Ctnna3</i> Deficiency Promotes Heart Regeneration by Enhancing Cardiomyocyte Proliferation in Neonatal Mice.\",\"authors\":\"Sha Zou, Wuhou Dai, Wufan Tao, Jifen Li, Zeyi Cheng, Hongyan Wang\",\"doi\":\"10.31083/FBL39676\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Heart regeneration requires renewal of lost cardiomyocytes. However, the mammalian heart loses its proliferative capacity soon after birth, and the molecular signaling underlying the loss of cardiac proliferation postnatally is not fully understood.</p><p><strong>Purpose: </strong>This study aimed to investigate the role of Catenin alpha 3 (<i>Ctnna3</i>), coding for alpha T catenin (αT-catenin) protein in regulating cardiomyocyte proliferation and heart regeneration during the neonatal period.</p><p><strong>Methods: </strong>Here we report that ablation of <i>Ctnna3</i> and highly expressed in hearts, accelerated heart regeneration following heart apex resection in neonatal mice.</p><p><strong>Results: </strong>Our results show that <i>Ctnna3</i> deficiency enhances cardiomyocyte proliferation in hearts from postnatal day 7 (P7) mice by upregulating Yes-associated protein (Yap) expression.</p><p><strong>Conclusion: </strong>Our study demonstrates that <i>Ctnna3</i> deficiency is sufficient to promote heart regeneration and cardiomyocyte proliferation in neonatal mice and indicates that functional interference of α-catenins might help to stimulate myocardial regeneration after injury.</p>\",\"PeriodicalId\":73069,\"journal\":{\"name\":\"Frontiers in bioscience (Landmark edition)\",\"volume\":\"30 7\",\"pages\":\"39676\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2025-07-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Frontiers in bioscience (Landmark edition)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.31083/FBL39676\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Frontiers in bioscience (Landmark edition)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.31083/FBL39676","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
Ctnna3 Deficiency Promotes Heart Regeneration by Enhancing Cardiomyocyte Proliferation in Neonatal Mice.
Background: Heart regeneration requires renewal of lost cardiomyocytes. However, the mammalian heart loses its proliferative capacity soon after birth, and the molecular signaling underlying the loss of cardiac proliferation postnatally is not fully understood.
Purpose: This study aimed to investigate the role of Catenin alpha 3 (Ctnna3), coding for alpha T catenin (αT-catenin) protein in regulating cardiomyocyte proliferation and heart regeneration during the neonatal period.
Methods: Here we report that ablation of Ctnna3 and highly expressed in hearts, accelerated heart regeneration following heart apex resection in neonatal mice.
Results: Our results show that Ctnna3 deficiency enhances cardiomyocyte proliferation in hearts from postnatal day 7 (P7) mice by upregulating Yes-associated protein (Yap) expression.
Conclusion: Our study demonstrates that Ctnna3 deficiency is sufficient to promote heart regeneration and cardiomyocyte proliferation in neonatal mice and indicates that functional interference of α-catenins might help to stimulate myocardial regeneration after injury.
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