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Anyone read up on below? Seen some places offering it. Epicardial FSTL1 reconstitution regenerates the adult mammalian heart
Ke Wei, Vahid Serpooshan, Cecilia Hurtado, Marta Diez-Cuñado, Mingming Zhao, Sonomi Maruyama, Wenhong Zhu, Giovanni Fajardo, Michela Noseda, Kazuto Nakamura, Xueying Tian, Qiaozhen Liu, Andrew Wang, Yuka Matsuura, Paul Bushway, Wenqing Cai, Alex Savchenko, Morteza Mahmoudi, Michael D. Schneider, Maurice J. B. van den Hoff, Manish J. Butte, Phillip C. Yang, Kenneth Walsh, Bin Zhou, Daniel Bernstein et al.
AffiliationsContributionsCorresponding author
Nature 525, 479–485 (24 September 2015) doi:10.1038/nature15372
Received 18 December 2013 Accepted 11 August 2015 Published online 16 September 2015 Corrected online 23 September 2015
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Abstract
Abstract• Change history• References• Author information• Extended data figures and tables• Supplementary information
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.
Ke Wei, Vahid Serpooshan, Cecilia Hurtado, Marta Diez-Cuñado, Mingming Zhao, Sonomi Maruyama, Wenhong Zhu, Giovanni Fajardo, Michela Noseda, Kazuto Nakamura, Xueying Tian, Qiaozhen Liu, Andrew Wang, Yuka Matsuura, Paul Bushway, Wenqing Cai, Alex Savchenko, Morteza Mahmoudi, Michael D. Schneider, Maurice J. B. van den Hoff, Manish J. Butte, Phillip C. Yang, Kenneth Walsh, Bin Zhou, Daniel Bernstein et al.
AffiliationsContributionsCorresponding author
Nature 525, 479–485 (24 September 2015) doi:10.1038/nature15372
Received 18 December 2013 Accepted 11 August 2015 Published online 16 September 2015 Corrected online 23 September 2015
Article
Citation
Reprints
Rights & permissions
Article metrics
Abstract
Abstract• Change history• References• Author information• Extended data figures and tables• Supplementary information
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.