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论文题目: Epicardial FSTL1 reconstitution regenerates the adult mammalian heart
英文论文题目: Epicardial FSTL1 reconstitution regenerates the adult mammalian heart
第一作者: Wei, K; Serpooshan, V; Hurtado, C; Diez-Cunado, M; Zhao, MM; Maruyama, S; Zhu, WH; Fajardo, G; Noseda, M; Nakamura, K; Tian, XY; Liu, QZ; Wang, A; Matsuura, Y; Bushway, P; Cai, WQ; Savchenko, A; Mahmoudi, M; Schneider, MD; van den Hoff, MJB; Butte, MJ; Yang, PC; Walsh, K; Zhou, B; Bernstein, D; Mercola, M; Ruiz-Lozano, P
英文第一作者: Wei, K; Serpooshan, V; Hurtado, C; Diez-Cunado, M; Zhao, MM; Maruyama, S; Zhu, WH; Fajardo, G; Noseda, M; Nakamura, K; Tian, XY; Liu, QZ; Wang, A; Matsuura, Y; Bushway, P; Cai, WQ; Savchenko, A; Mahmoudi, M; Schneider, MD; van den Hoff, MJB; Butte, MJ; Yang, PC; Walsh, K; Zhou, B; Bernstein, D; Mercola, M; Ruiz-Lozano, P
联系作者: Ruiz-Lozano, P (reprint author), Stanford Univ, Sch Med, Stanford Cardiovasc Inst, 300 Pasteur Dr, Stanford, CA 94305 USA.
英文联系作者: Ruiz-Lozano, P (reprint author), Stanford Univ, Sch Med, Stanford Cardiovasc Inst, 300 Pasteur Dr, Stanford, CA 94305 USA.
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发表年度: 2015
卷: 525
期: 7570
页码: 479-+
摘要: The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Herewe 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.
英文摘要: The elucidation of factors that activate the regeneration of the adult mammalian heart is of major scientific and therapeutic importance. Herewe 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.
刊物名称: NATURE
英文刊物名称: NATURE
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学科: Science & Technology - Other Topics
英文学科: Science & Technology - Other Topics
影响因子: 41.456
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论文类别: Review
英文论文类别: Review
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