Abstract

Essential muscular organ that provides the whole body with oxygen and nutrients, the heart is the first organ to function during embryonic development. Cardiovascular diseases, including acquired and congenital heart defects, are the leading cause of mortality in industrialized countries. Fibroblast Growth Factors (FGFs) are involved in a variety of cellular responses including proliferation, differentiation, and migration. Among the 22 human/mouse FGFs, the secreted FGF10 ligand through the binding of its specific receptors (FGFR1b and FGFR2b) and subsequent activation of downstream signaling is known to play essential role in cardiac development, homeostasis and disease. FGF10 is one of the major marker of the early cardiac progenitor cells and a crucial regulator of differentiated cardiomyocyte proliferation in the developing embryo. Increasing evidence support the hypothesis that a detailed understanding of developmental processes is essential to identify targets for cardiac repair and regeneration. Indeed the activation of resident cardiomyocyte proliferation together with the injection of cardiac progenitors represent the most promising therapeutical strategies for cardiac regenerative medicine. The recent findings showing that FGF10 promotes adult cardiomyocyte cell cycle reentry and directs stem cell differentiation and cell reprogramming toward the cardiogenic lineage provide new insights into therapeutical strategies for cardiac regeneration and repair.

Highlights

  • Frontiers in GeneticsReceived: 27 September 2018 Accepted: 15 November 2018 Published: 28 November 2018. Citation: Hubert F, Payan SM and Rochais F (2018) FGF10 Signaling in Heart Development, Homeostasis, Disease and Repair

  • The heart is an essential muscular organ that pumps blood and provides the whole body with oxygen and nutrients

  • FGF3 and FGF10 have been shown to play redundant and dosage sensitive requirement during heart tube elongation (Urness et al, 2011). All these studies highlight that critical Fibroblast Growth Factors (FGFs) dosage, including FGF10, is crucial for second heart field (SHF) proliferation and deployment and for normal cardiac morphogenesis

Read more

Summary

Frontiers in Genetics

Received: 27 September 2018 Accepted: 15 November 2018 Published: 28 November 2018. Citation: Hubert F, Payan SM and Rochais F (2018) FGF10 Signaling in Heart Development, Homeostasis, Disease and Repair. Essential muscular organ that provides the whole body with oxygen and nutrients, the heart is the first organ to function during embryonic development. Among the 22 human/mouse FGFs, the secreted FGF10 ligand through the binding of its specific receptors (FGFR1b and FGFR2b) and subsequent activation of downstream signaling is known to play essential role in cardiac development, homeostasis and disease. FGF10 is one of the major marker of the early cardiac progenitor cells and a crucial regulator of differentiated cardiomyocyte proliferation in the developing embryo. The activation of resident cardiomyocyte proliferation together with the injection of cardiac progenitors represent the most promising therapeutical strategies for cardiac regenerative medicine. The recent findings showing that FGF10 promotes adult cardiomyocyte cell cycle reentry and directs stem cell differentiation and cell reprogramming toward the cardiogenic lineage provide new insights into therapeutical strategies for cardiac regeneration and repair

INTRODUCTION
CONCLUSION
Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.