Resetting the epigenome for heart regeneration. (October 2016)

• Record Type: Journal Article
• Authors: Quaife-Ryan, Gregory A.; Sim, Choon Boon; Porrello, Enzo R.; Hudson, James E.
• Is Part Of: Seminars in cell & developmental biology. Volume 58(2016)
• Page Start: 2
• Page End: 13
• Publication Date: 2016-10
• Subjects: 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 Jumonji domain-containing protein 3 -- KDMs histone lysine demethylases -- lncRNAs long non-coding RNAs -- Mhrt Myheart -- miRNAs microRNAs -- Myh myosin heavy chain -- PRC2 polycomb repressive complex 2 -- PSCs pluripotent stem cells -- PTM post-translational modification -- SIRTs sirtuins -- SMYD1 SET and MYND domain containing 1 -- Srf serum response factor -- TET ten-eleven translocation -- TGFβ transforming growth factor beta -- TFs transcription factors -- UTX ubiquitously transcribed tetratricopeptide repeat, X chromosome; Epigenetics -- Reprogramming -- Heart regeneration -- Cardiomyocyte proliferation -- Cardiac development; Cytology -- Periodicals; Developmental biology -- Periodicals; 571.6
• DOI: 10.1016/j.semcdb.2015.12.021
• Languages: English
• ISSNs: 1084-9521

Abstract

Abstract: 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.