科学家们确认了一组分子信号，这些信号可激活包围哺乳动物心脏的保护性的，及可能是修复性的组织层。这一发现可能最终会带来修复心脏损害的新策略。
该被称作心外膜的组织在发育中会提供必需的生长因子和干细胞。它在成年期会处于休眠状态，但在心脏受损时会被重新激活。这一反应重新激活了那些在发育时帮助心脏生长的基因，但是引起这一过程的机制则一直是未知的。
Guo Huang及其同事在研究小鼠模型时发现，所谓的C/EBP转录因子激活了发育和损伤时的心外膜。阻断受伤心脏的心外膜中的C/EBP信号传导可减少炎症并改善心脏功能。（生物谷Bioon.com）
doi: 10.1126/science.1229765
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PMID:
C/EBP Transcription Factors Mediate Epicardial Activation During Heart Development and Injury
Guo N. Huang, Jeffrey E. Thatcher, John McAnally, Yongli Kong, Xiaoxia Qi, Wei Tan, J. Michael DiMaio, James F. Amatruda, Robert D. Gerard, Joseph A. Hill, Rhonda Bassel-Duby, Eric N. Olson
The epicardium encapsulates the heart and functions as a source of multipotent progenitor cells and paracrine factors essential for cardiac development and repair. Injury of the adult heart results in reactivation of a developmental gene program in the epicardium, but the transcriptional basis of epicardial gene expression has not been delineated. We established a mouse embryonic heart organ culture and gene expression system that facilitated the identification of epicardial enhancers activated during heart development and injury. Epicardial activation of these enhancers depends on a combinatorial transcriptional code centered on CCAAT/enhancer binding protein (C/EBP) transcription factors. Disruption of C/EBP signaling in the adult epicardium reduced injury-induced neutrophil infiltration and improved cardiac function. These findings reveal a transcriptional basis for epicardial activation and heart injury, providing a platform for enhancing cardiac regeneration.
