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Phases and Mechanisms of Embryonic Cardiomyocyte Proliferation and Ventricular Wall Morphogenesis

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A Correction to this article was published on 04 November 2019

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Abstract

If viewed as a movie, heart morphogenesis appears to unfold in a continuous and seamless manner. At the mechanistic level, however, a series of discreet and separable processes sequentially underlie heart development. This is evident in examining the expansion of the ventricular wall, which accounts for most of the contractile force of each heartbeat. Ventricular wall expansion is driven by cardiomyocyte proliferation coupled with a morphogenetic program that causes wall thickening rather than lengthening. Although most studies of these processes have focused on heart-intrinsic processes, it is increasingly clear that extracardiac events influence or even direct heart morphogenesis. In this review, we specifically consider mechanisms responsible for coordinating cardiomyocyte proliferation and ventricular wall expansion in mammalian development, relying primarily on studies from mouse development where a wealth of molecular and genetic data have been accumulated.

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Change history

  • 04 November 2019

    The original version of this article unfortunately contained a mistake. In reviewing the phenotype associated with Mapk14 (p38alpha MAPK) mutation as evaluated by Adams et al. (2000) using tetraploid aggregation chimeric embryos, the authors mistakenly stated that rescue of embryo lethality was short-lived and that embryos died two days later of non-placenta-related causes. In fact, as reported by Adams et al. (2000), when the placental defect of global null embryos was rescued, p38alpha(−/−) embryos developed to term and were normal in appearance. The authors apologize for the error.

  • 04 November 2019

    The original version of this article unfortunately contained a mistake. In reviewing the phenotype associated with Mapk14 (p38alpha MAPK) mutation as evaluated by Adams et al. (2000) using tetraploid aggregation chimeric embryos, the authors mistakenly stated that rescue of embryo lethality was short-lived and that embryos died two days later of non-placenta-related causes. In fact, as reported by Adams et al. (2000), when the placental defect of global null embryos was rescued, p38alpha(���/���) embryos developed to term and were normal in appearance. The authors apologize for the error.

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Funding

This review was supported in part by The Magee Prize, Grant #MP001, from the Magee-Womens Research Institute and the Richard King Mellon Foundation, given to YB, MH, and HMS, and by NIH Grant HL070123 provided to HMS.

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Correspondence to Henry M. Sucov.

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Barak, Y., Hemberger, M. & Sucov, H.M. Phases and Mechanisms of Embryonic Cardiomyocyte Proliferation and Ventricular Wall Morphogenesis. Pediatr Cardiol 40, 1359–1366 (2019). https://doi.org/10.1007/s00246-019-02164-6

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