Nature2015，525：479-485報(bào)道，受傷后心外膜也許能在某種程度上保持成年心肌的功能，可能是通過提供肌源性祖細(xì)胞來發(fā)揮這種作用的。這項(xiàng)研究發(fā)現(xiàn)，分泌出的因子follistatin-like 1(FSTL1)是一個(gè)再生因子，它正常情況下存在于健康的心外膜中，但在心肌梗塞之后會(huì)失去，這是受傷降低哺乳動(dòng)物心臟的再生能力的一個(gè)機(jī)制。用一種人造心外膜生物材料進(jìn)行FSTL1的重建，改善了心肌梗塞動(dòng)物模型的心臟功能，同時(shí)也有證據(jù)表明心肌細(xì)胞再生適合進(jìn)行臨床應(yīng)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.