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Epicardial FSTL1 reconstitution regenerates the adult mammalian heart

Author

Listed:
  • Ke Wei

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Vahid Serpooshan

    (Stanford University School of Medicine)

  • Cecilia Hurtado

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Marta Diez-Cuñado

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute
    Stanford University School of Medicine)

  • Mingming Zhao

    (Stanford University School of Medicine)

  • Sonomi Maruyama

    (Whitaker Cardiovascular Institute, Boston University School of Medicine)

  • Wenhong Zhu

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Giovanni Fajardo

    (Stanford University School of Medicine)

  • Michela Noseda

    (Imperial College London, Faculty of Medicine, Imperial Centre for Translational and Experimental Medicine)

  • Kazuto Nakamura

    (Whitaker Cardiovascular Institute, Boston University School of Medicine)

  • Xueying Tian

    (Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, and Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences)

  • Qiaozhen Liu

    (Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, and Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences)

  • Andrew Wang

    (Stanford University School of Medicine)

  • Yuka Matsuura

    (Stanford University School of Medicine)

  • Paul Bushway

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Wenqing Cai

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Alex Savchenko

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Morteza Mahmoudi

    (Stanford University School of Medicine
    Nanotechnology Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences)

  • Michael D. Schneider

    (Imperial College London, Faculty of Medicine, Imperial Centre for Translational and Experimental Medicine)

  • Maurice J. B. van den Hoff

    (Academic Medical Center. Dept Anatomy, Embryology and Physiology)

  • Manish J. Butte

    (Stanford University School of Medicine)

  • Phillip C. Yang

    (Stanford University School of Medicine)

  • Kenneth Walsh

    (Whitaker Cardiovascular Institute, Boston University School of Medicine)

  • Bin Zhou

    (Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, and Shanghai Institutes for Biological Sciences, Graduate School of the Chinese Academy of Sciences, Chinese Academy of Sciences
    CAS Center for Excellence in Brain Science, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences)

  • Daniel Bernstein

    (Stanford University School of Medicine)

  • Mark Mercola

    (University of California, San Diego
    Sanford-Burnham-Prebys Medical Discovery Institute)

  • Pilar Ruiz-Lozano

    (Stanford University School of Medicine)

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.

Suggested Citation

  • 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 & An, 2015. "Epicardial FSTL1 reconstitution regenerates the adult mammalian heart," Nature, Nature, vol. 525(7570), pages 479-485, September.
    • Handle: RePEc:nat:nature:v:525:y:2015:i:7570:d:10.1038_nature15372
    DOI: 10.1038/nature15372
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    Cited by:

    1. Yu Xia & Sierra Duca & Björn Perder & Friederike Dündar & Paul Zumbo & Miaoyan Qiu & Jun Yao & Yingxi Cao & Michael R. M. Harrison & Lior Zangi & Doron Betel & Jingli Cao, 2022. "Activation of a transient progenitor state in the epicardium is required for zebrafish heart regeneration," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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