Nichole M McMullen, Gerard J. Gaspard, K. Pasumarthi
{"title":"心肌细胞周期的再激活:心肌再生的一种潜在途径","authors":"Nichole M McMullen, Gerard J. Gaspard, K. Pasumarthi","doi":"10.1002/SITA.200400050","DOIUrl":null,"url":null,"abstract":"Regulation of cardiomyocyte cell cycle appears to be more complex in mammals compared to the lower vertebrates. Cardiomyocytes from the adult newt and zebrafish can proliferate in response to myocardial injury and regenerate the damaged area. In contrast, cardiomyocytes in the mammalian heart cease to proliferate soon after birth. This limits the ability of the mammalian heart to regenerate the damaged myocardium following heart disease. It is believed that increasing the number of myocytes in a diseased heart can decrease scar formation and improve myocardial function. To this end, reactivation of cell cycle in the surviving myocardium may have therapeutic value in the treatment of heart disease. Here we provide a summary of studies describing myocyte cell cycle activity during development and disease, mechanisms of cell cycle exit in the adult heart and genetic modulations affecting cardiomyocyte cell cycle activity. Further, we discuss the potential utility of myocyte cell cycle reactivation in cardiac regeneration as well as improvement of myocardial function.","PeriodicalId":88702,"journal":{"name":"Signal transduction","volume":"57 8","pages":"126-141"},"PeriodicalIF":0.0000,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/SITA.200400050","citationCount":"4","resultStr":"{\"title\":\"Reactivation of cardiomyocyte cell cycle: A potential approach for myocardial regeneration\",\"authors\":\"Nichole M McMullen, Gerard J. Gaspard, K. Pasumarthi\",\"doi\":\"10.1002/SITA.200400050\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Regulation of cardiomyocyte cell cycle appears to be more complex in mammals compared to the lower vertebrates. Cardiomyocytes from the adult newt and zebrafish can proliferate in response to myocardial injury and regenerate the damaged area. In contrast, cardiomyocytes in the mammalian heart cease to proliferate soon after birth. This limits the ability of the mammalian heart to regenerate the damaged myocardium following heart disease. It is believed that increasing the number of myocytes in a diseased heart can decrease scar formation and improve myocardial function. To this end, reactivation of cell cycle in the surviving myocardium may have therapeutic value in the treatment of heart disease. Here we provide a summary of studies describing myocyte cell cycle activity during development and disease, mechanisms of cell cycle exit in the adult heart and genetic modulations affecting cardiomyocyte cell cycle activity. Further, we discuss the potential utility of myocyte cell cycle reactivation in cardiac regeneration as well as improvement of myocardial function.\",\"PeriodicalId\":88702,\"journal\":{\"name\":\"Signal transduction\",\"volume\":\"57 8\",\"pages\":\"126-141\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2005-08-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1002/SITA.200400050\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Signal transduction\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/SITA.200400050\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Signal transduction","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/SITA.200400050","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Reactivation of cardiomyocyte cell cycle: A potential approach for myocardial regeneration
Regulation of cardiomyocyte cell cycle appears to be more complex in mammals compared to the lower vertebrates. Cardiomyocytes from the adult newt and zebrafish can proliferate in response to myocardial injury and regenerate the damaged area. In contrast, cardiomyocytes in the mammalian heart cease to proliferate soon after birth. This limits the ability of the mammalian heart to regenerate the damaged myocardium following heart disease. It is believed that increasing the number of myocytes in a diseased heart can decrease scar formation and improve myocardial function. To this end, reactivation of cell cycle in the surviving myocardium may have therapeutic value in the treatment of heart disease. Here we provide a summary of studies describing myocyte cell cycle activity during development and disease, mechanisms of cell cycle exit in the adult heart and genetic modulations affecting cardiomyocyte cell cycle activity. Further, we discuss the potential utility of myocyte cell cycle reactivation in cardiac regeneration as well as improvement of myocardial function.