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JCDD
Special Issues
Myocardial Reprogramming in Development and Regeneration
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Myocardial Reprogramming in Development and Regeneration

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425).

Deadline for manuscript submissions: closed (1 May 2016) | Viewed by 19650

Special Issue Editors

Dr. Sean M. Wu

E-Mail Website
Guest Editor
Lokey Stem Cell Building, G1120A, Stanford Cardiovascular Institute, 265, Campus Dr, Stanford, CA 94305, USA
Interests: cardiac progenitor cell; cardiac development; transcriptional regulation; Nkx2-5; myocardial regeneration; induced pluripotent stem cell
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Neil C. Chi

E-Mail Website
Guest Editor
Institute for Genomic Medicine, University of California San Diego, San Diego, CA 92093-0613J, USA
Interests: regenerative animal model systems; human pluripotent stem cells; myocardial regeneration; cardiovascular development

Special Issue Information

Dear Colleagues,

This Special Issue of JCDD is focused on the topic of “Myocardial Reprogramming in Development and Regeneration”, which we believe to be of significant interest to many cardiac developmental biologists, stem cell biologists, and clinician scientists seeking to employ regenerative approaches to cardiovascular diseases. Recent advances in pluripotent stem cell reprogramming and our improved understanding of the key transcriptional regulatory events driving cardiac lineage commitment and differentiation have opened numerous areas of investigation from in vitro cardiac disease modeling to direct cardiomyocyte reprogramming and cardiovascular cell transplantation therapy. These exciting research pursuits have also raised important questions regarding the most stringent criteria that should be used to define a true functional cardiomyocyte and the challenges that must be confronted in order to generate a fully mature adult cardiomyocyte that is able to integrate into the heart to improve overall cardiac function and long-term survival. In this rapidly evolving research field, we hope to illustrate the promises and the pitfalls of cardiac reprogramming for normal development, and highlight key opportunities where this approach may lead to promising new therapies for cardiac regeneration.

Prof. Dr. Sean M. Wu
Prof. Dr. Neil C. Chi
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

 

Keywords

  • Myocardial development
  • Transcriptional regulation
  • Lineage reprogramming
  • Atrial and ventricular cardiomyocyte
  • Myocardial regeneration
  • Cardiomyocyte proliferation
  • Cell therapy
  • Pluripotent stem cells

Published Papers (3 papers)

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Research

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3705 KiB  
Article
Collagenolytic Activity Is Associated with Scar Resolution in Zebrafish Hearts after Cryoinjury
by Laurent Gamba, Armaan Amin-Javaheri, Jieun Kim, David Warburton and Ching-Ling Lien
J. Cardiovasc. Dev. Dis. 2017, 4(1), 2; https://doi.org/10.3390/jcdd4010002 - 24 Feb 2017
Cited by 14 | Viewed by 6738
Abstract
Myocardial infarction is the major cause of cardiac injury in western countries and can result in a massive loss of heart cells, leading eventually to heart failure. A fibrotic collagen-rich scar may prevent ventricular wall rupture, but also may result in heart failure [...] Read more.
Myocardial infarction is the major cause of cardiac injury in western countries and can result in a massive loss of heart cells, leading eventually to heart failure. A fibrotic collagen-rich scar may prevent ventricular wall rupture, but also may result in heart failure because of its stiffness. In zebrafish, cardiac cryoinjury triggers a fibrotic response and scarring. Unlike with mammals, zebrafish heart has the striking ability to regenerate and to resolve the scar. Thus, understanding the mechanisms of scar resolution in zebrafish heart might facilitate the design of new therapeutic approaches to improve the recovery of patients. To visualize the collagenolytic activity within the zebrafish heart following cryoinjury, we used an in situ collagen zymography assay. We detected expression of mmp2 and mmp14a and these matrix metalloproteinases might contribute to the collagenase activity. Collagenolytic activity was present in the wound area, but decreased as the myocardium regenerated. Comparison with neonatal mouse hearts that failed to regenerate after transmural cryoinjury revealed a similar collagenolytic activity in the scar. These findings suggest that collagenolytic activity may be key to how the zebrafish heart resolves its scar; however, it is not sufficient in mouse hearts that lack efficient myocardial regeneration. Full article
(This article belongs to the Special Issue Myocardial Reprogramming in Development and Regeneration)
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Review

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Review
The Function of the MEF2 Family of Transcription Factors in Cardiac Development, Cardiogenomics, and Direct Reprogramming
by Cody A. Desjardins and Francisco J. Naya
J. Cardiovasc. Dev. Dis. 2016, 3(3), 26; https://doi.org/10.3390/jcdd3030026 - 11 Aug 2016
Cited by 61 | Viewed by 7118
Abstract
Proper formation of the mammalian heart requires precise spatiotemporal transcriptional regulation of gene programs in cardiomyocytes. Sophisticated regulatory networks have evolved to not only integrate the activities of distinct transcription factors to control tissue-specific gene programs but also, in many instances, to incorporate [...] Read more.
Proper formation of the mammalian heart requires precise spatiotemporal transcriptional regulation of gene programs in cardiomyocytes. Sophisticated regulatory networks have evolved to not only integrate the activities of distinct transcription factors to control tissue-specific gene programs but also, in many instances, to incorporate multiple members within these transcription factor families to ensure accuracy and specificity in the system. Unsurprisingly, perturbations in this elaborate transcriptional circuitry can lead to severe cardiac abnormalities. Myocyte enhancer factor–2 (MEF2) transcription factor belongs to the evolutionarily conserved cardiac gene regulatory network. Given its central role in muscle gene regulation and its evolutionary conservation, MEF2 is considered one of only a few core cardiac transcription factors. In addition to its firmly established role as a differentiation factor, MEF2 regulates wide variety of, sometimes antagonistic, cellular processes such as cell survival and death. Vertebrate genomes encode multiple MEF2 family members thereby expanding the transcriptional potential of this core transcription factor in the heart. This review highlights the requirement of the MEF2 family and their orthologs in cardiac development in diverse animal model systems. Furthermore, we describe the recently characterized role of MEF2 in direct reprogramming and genome-wide cardiomyocyte gene regulation. A thorough understanding of the regulatory functions of the MEF2 family in cardiac development and cardiogenomics is required in order to develop effective therapeutic strategies to repair the diseased heart. Full article
(This article belongs to the Special Issue Myocardial Reprogramming in Development and Regeneration)
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201 KiB  
Review
Vascular Development and Regeneration in the Mammalian Heart
by Oscar M. Leung, Bin Zhou and Kathy O. Lui
J. Cardiovasc. Dev. Dis. 2016, 3(2), 23; https://doi.org/10.3390/jcdd3020023 - 16 Jun 2016
Cited by 5 | Viewed by 5352
Abstract
Cardiovascular diseases including coronary artery disease are the leading cause of death worldwide. Unraveling the developmental origin of coronary vessels could offer important therapeutic implications for treatment of cardiovascular diseases. The recent identification of the endocardial source of coronary vessels reveals a heterogeneous [...] Read more.
Cardiovascular diseases including coronary artery disease are the leading cause of death worldwide. Unraveling the developmental origin of coronary vessels could offer important therapeutic implications for treatment of cardiovascular diseases. The recent identification of the endocardial source of coronary vessels reveals a heterogeneous origin of coronary arteries in the adult heart. In this review, we will highlight recent advances in finding the sources of coronary vessels in the mammalian heart from lineage-tracing models as well as differentiation studies using pluripotent stem cells. Moreover, we will also discuss how we induce neovascularization in the damaged heart through transient yet highly efficient expression of VEGF-modified mRNAs as a potentially therapeutic delivery platform. Full article
(This article belongs to the Special Issue Myocardial Reprogramming in Development and Regeneration)
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