Resetting the epigenome for heart regeneration.

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• 作者：Gregory A. Quaife-Ryan¹ ; Choon Boon Sim¹ ; Enzo R. Porrello ; ^{e.porrello@uq.edu.au" class="auth_mail" title="E-mail the corresponding author} ; James E. Hudson ; ^{j.hudson@uq.edu.au" class="auth_mail" title="E-mail the corresponding author}
• 关键词：BMP ; bone morphogenetic protein ; Bvht ; braveheart ; CBP ; CREB-binding protein ; Cdkn ; cyclin dependent kinase inhibitor ; DOT1L ; disruptor of telomeric silencing-1 ; DNMTs ; DNA methyltransferases ; eRNAs ; ; enhancer RNAs ; ESCs ; embryonic stem cells ; FGF ; fibroblast growth factor ; FOX ; forkhead box ; Gcn5 ; general control of amino acid synthesis protein 5 ; HATs ; histone acetyl transferases ; HDACs ; histone deacteylases ; H3K27 ; histone 3 ; lysine 27 ; HMTs ; histone methyltransferases ; Jmj ; Jumonji ; JMJD3
• 刊名：Seminars in Cell & Developmental Biology
• 出版年：2016
• 出版时间：October 2016
• 年：2016
• 卷：58
• 期：Complete
• 页码：2-13
• 全文大小：2154 K

文摘

In contrast to adults, recent evidence suggests that neonatal mice are able to regenerate following cardiac injury. This regenerative capacity is reliant on robust induction of cardiomyocyte proliferation, which is required for faithful regeneration of the heart following injury. However, cardiac regenerative potential is lost as cardiomyocytes mature and permanently withdraw from the cell cycle shortly after birth. Recently, a handful of factors responsible for the regenerative disparity between the adult and neonatal heart have been identified, but the proliferative response of adult cardiomyocytes following modulation of these factors rarely reaches neonatal levels. The inefficient re-induction of proliferation in adult cardiomyocytes may be due to the epigenetic landscape, which drastically changes during cardiac development and maturation. In this review, we provide an overview of the role of epigenetic modifiers in developmental processes related to cardiac regeneration. We propose an epigenetic framework for heart regeneration whereby adult cardiomyocyte identity requires resetting to a neonatal-like state to facilitate cell cycle re-entry and regeneration following cardiac injury.