Cited by 514Congenital heart defects researchTissue Engineering and Regenerative MedicineNeurogenesis and neuroplasticity mechanisms

Mending broken hearts: cardiac development as a basis for adult heart regeneration and repair

Open access
Xin, Mei, Olson, Eric N., Bassel-Duby, Rhonda·2013·Nature Reviews Molecular Cell Biology

Abstract

As the adult mammalian heart has limited potential for regeneration and repair, the loss of cardiomyocytes during injury and disease can result in heart failure and death. The cellular processes and regulatory mechanisms involved in heart growth and development can be exploited to repair the injured adult heart through 'reawakening' pathways that are active during embryogenesis. Heart function has been restored in rodents by reprogramming non-myocytes into cardiomyocytes, by expressing transcription factors (GATA4, HAND2, myocyte-specific enhancer factor 2C (MEF2C) and T-box 5 (TBX5)) and microRNAs (miR-1, miR-133, miR-208 and miR-499) that control cardiomyocyte identity. Stimulating cardiomyocyte dedifferentiation and proliferation by activating mitotic signalling pathways involved in embryonic heart growth represents a complementary approach for heart regeneration and repair. Recent advances in understanding the mechanistic basis of heart development offer exciting opportunities for effective therapies for heart failure.

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Crossref · 10.1038/nrm3619

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  • Yap loss- or gain-of-function in the embryonic heart is frequently lethal.

    “Several studies show that Yap loss- or gainof-function in the embryonic heart is frequently lethal (reviewed by (84, 141, 155)).”

    From The Hippo signal transduction network for exercise physiologists (2016) · cites this paper as [155]

    The section “Inactivation of Hippo signalling promotes proliferation” reports that Yap deletion in the embryonic heart caused embryonic lethality. It says YAP gain of function stimulates cardiomyocyte proliferation, but does not say it is lethal. The review also does not establish that lethality occurs frequently. (LLM, conf=0.88)

    Experimental — accuracy not yet measured

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Authors
Xin, M., Olson, E. N., & Bassel-Duby, R.
Affiliations
The University of Texas Southwestern Medical Center (US)
Corresponding author
Olson, Eric N.
Venue
Nature Reviews Molecular Cell Biology
Published
2013-07-10
Volume
14
Issue
8
Pages
529-541
ISSN
  • 1471-0072 (ISSN-L)
  • 1471-0080
OpenAlex
W2015644748
Cited by
514
References
114
Citations by year
2026: 17 · 2025: 24 · 2024: 37 · 2023: 34 · 2022: 34 · 2021: 34 · 2020: 42 · 2019: 47 · 2018: 51 · 2017: 47 · 2016: 47 · 2015: 55 · 2014: 38 · 2013: 5 · 2012: 1
FWCI
4.54
Type
journal article
Language
en
Open access
Locations
  • Nature Reviews Molecular Cell Biology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • Welch Foundation
  • Aurora Foundation
  • National Institutes of Health (5u01hl100401-07)
  • National Heart, Lung, and Blood Institute (R01HL111665, R01HL077439, U01-HL-100401, R01HL093039)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK099653)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
  • Health Sciences › Medicine › Surgery › Tissue Engineering and Regenerative Medicine
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
Keywords
cardiac regeneration, heart development, heart failure, cardiomyocyte dedifferentiation, cardiomyocyte proliferation, transcription factors, microRNA, cardiac repair
MeSH terms
Adult, Animals, Heart, Humans, Models, Biological, Regeneration, Wound Healing, Myocytes, Cardiac, Regenerative Medicine, Embryonic Development

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