| Literature DB >> 26375005 |
Ke Wei1,2, Vahid Serpooshan3, Cecilia Hurtado1,2, Marta Diez-Cuñado1,2,3, Mingming Zhao3, Sonomi Maruyama4, Wenhong Zhu1,2, Giovanni Fajardo3, Michela Noseda5, Kazuto Nakamura4, Xueying Tian6, Qiaozhen Liu6, Andrew Wang3, Yuka Matsuura3, Paul Bushway1,2, Wenqing Cai1,2, Alex Savchenko1,2, Morteza Mahmoudi3,7, Michael D Schneider5, Maurice J B van den Hoff8, Manish J Butte3, Phillip C Yang3, Kenneth Walsh4, Bin Zhou6,9, Daniel Bernstein3, Mark Mercola1,2, Pilar Ruiz-Lozano3.
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.Entities:
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Year: 2015 PMID： 26375005 PMCID： PMC4762253 DOI： 10.1038/nature15372
Source DB: PubMed Journal: Nature ISSN： 0028-0836 Impact factor: 49.962