Epigenetic and lncRNA regulation of cardiac pathophysiology.
Epigenetic and lncRNA regulation of cardiac pathophysiology.
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DOI：
10.1016/j.bbamcr.2016.03.005
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发表时间：
2016-07
期刊：
影响因子：
--
通讯作者：
Han P
中科院分区：
文献类型：
--
作者：
Chang CP;Han P
我们的发育研究提供了对成人心力衰竭发病机制的深入了解。这些研究揭示了胎儿心肌细胞和病理应激的成年心肌细胞在染色质调节水平上的机制联系。在胚胎中，心肌细胞内的染色质调节因子响应发育信号来编程心脏基因表达，从而促进细胞增殖并抑制细胞过早分化。在新生儿期，心肌细胞中这些发育染色质调节因子的活性迅速关闭，与细胞增殖的停止和细胞向成年成熟的分化相一致。当成熟的心脏受到病理性应激时，胚胎中心肌细胞发育所必需的染色质调节因子会被重新激活，从而引发基因重编程至胎儿样状态和病理性心脏肥大。此外，在染色质调控和心脏基因表达的研究中，我们发现了一种长非编码RNA，它与染色质重塑因子相互作用，调节心脏对环境变化的反应。本文是题为“心肌细胞生物学：心脏中发育和环境线索的整合”特刊的一部分，由 Marcus Schaub 和 Hughes Abriel 编辑。
Our developmental studies provide an insight into the pathogenesis of heart failure in adults. These studies reveal a mechanistic link between fetal cardiomyocytes and pathologically stressed adult cardiomyocytes at the level of chromatin regulation. In embryos, chromatin-regulating factors within the cardiomyocytes respond to developmental signals to program cardiac gene expression to promote cell proliferation and inhibit premature cell differentiation. In the neonatal period, the activity of these developmental chromatin regulators is quickly turned off in cardiomyocytes, coinciding with the cessation of cell proliferation and advance in cell differentiation toward adult maturity. When the mature hearts are pathologically stressed, those chromatin regulators essential for cardiomyocyte development in embryos are reactivated, triggering gene reprogramming to a fetal-like state and pathological cardiac hypertrophy. Furthermore, in the study of chromatin regulation and cardiac gene expression, we identified a long noncoding RNA that interacts with chromatin remodeling factor to regulate the cardiac response to environmental changes. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel.
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