Nature2015，525：479-485报道，受伤后心外膜也许能在某种程度上保持成年心肌的功能，可能是通过提供肌源性祖细胞来发挥这种作用的。这项研究发现，分泌出的因子follistatin-like 1(FSTL1)是一个再生因子，它正常情况下存在于健康的心外膜中，但在心肌梗塞之后会失去，这是受伤降低哺乳动物心脏的再生能力的一个机制。用一种人造心外膜生物材料进行FSTL1的重建，改善了心肌梗塞动物模型的心脏功能，同时也有证据表明心肌细胞再生适合进行临床应用。

Epicardial FSTL1 reconstitution regenerates the adult mammalian heart

Abstract

The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Here we found that epicardial cells contain a potent cardiogenic activity identified as follistatin-like 1 (Fstl1). Epicardial Fstl1 declines following myocardial infarction and is replaced by myocardial expression. Myocardial Fstl1 does not promote regeneration, either basally or upon transgenic overexpression. Application of the human Fstl1 protein (FSTL1) via an epicardial patch stimulates cell cycle entry and division of pre-existing cardiomyocytes, improving cardiac function and survival in mouse and swine models of myocardial infarction. The data suggest that the loss of epicardial FSTL1 is a maladaptive response to injury, and that its restoration would be an effective way to reverse myocardial death and remodelling following myocardial infarction in humans.