Abstract
Cardiac myocytes (CMs) proliferate robustly during fetal life but withdraw permanently from the cell cycle soon after birth and undergo terminal differentiation. This cell cycle exit is associated with the upregulation of a host of adult cardiac-specific genes. The vast majority of adult CMs (ACMs) do not reenter cell cycle even if subjected to mitogenic stimuli. The basis for this irreversible cell cycle exit is related to the stable silencing of cell cycle genes specifically involved in the progression of G2/M transition and cytokinesis. Studies have begun to clarify the molecular basis for this stable gene repression and have identified epigenetic and chromatin structural changes in this process. In this review, we summarize the current understanding of epigenetic regulation of CM cell cycle and cardiac-specific gene expression with a focus on histone modifications and the role of retinoblastoma family members.
Highlights
The fetal heart increases in size throughout development via proliferation of Cardiac myocytes (CMs) but switches to mainly hypertrophic growth of CMs with limited proliferation soon after birth, undergoing terminal differentiation which is associated with permanent cell cycle exit (Ahuja et al, 2007; Mollova et al, 2013; Naqvi et al, 2014)
We summarize the current understanding of epigenetic regulation of CM cell cycle and cardiac-specific gene expression with a focus on histone modifications and the role of retinoblastoma family members
The fetal heart increases in size throughout development via proliferation of CMs but switches to mainly hypertrophic growth of CMs with limited proliferation soon after birth, undergoing terminal differentiation which is associated with permanent cell cycle exit (Ahuja et al, 2007; Mollova et al, 2013; Naqvi et al, 2014)
Summary
The fetal heart increases in size throughout development via proliferation of CMs but switches to mainly hypertrophic growth of CMs with limited proliferation soon after birth, undergoing terminal differentiation which is associated with permanent cell cycle exit (Ahuja et al, 2007; Mollova et al, 2013; Naqvi et al, 2014). We summarize the current understanding of epigenetic regulation of CM cell cycle and cardiac-specific gene expression with a focus on histone modifications and the role of retinoblastoma family members.
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