Special Issue "Highlights of the 2018 Marseille Meeting of the ESC Working Group on Development, Anatomy, and Pathology"

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

Deadline for manuscript submissions: 31 October 2019

Special Issue Editors

Guest Editor
Dr. Stephane Zaffran

Aix Marseille Université, INSERM U1251, MMG, Marseille, France
Website | E-Mail
Interests: developmental biology; cardiac and cardiovascular systems; pathology
Guest Editor
Dr. Robert G. Kelly

Developmental Biology Institute of Marseille, CNRS UMR 7288, Aix-Marseille University, France
Website | E-Mail
Interests: early heart development; cardiac progenitor cells; pharyngeal development; outflow tract morphogenesis; ventricular conduction system; craniofacial myogenesis; T-box genes

Special Issue Information

Dear Colleagues,

A forthcoming Special Issue of the Journal of Cardiovascular Development and Disease will be dedicated to papers and reviews stemming from the Marseille Cardiovascular Development Meeting, to be held at the Palais du Pharo in Marseille, France from 22–24 October, 2018.

The Marseille Cardiovascular Development Meeting, supported by JCDD, is the annual conference of the European Society of Cardiology Working Group on Development, Anatomy, and Pathology. A broad range of topics and animal models will be included in a highly interactive forum, spanning from cardiac progenitor cells in the early embryo through to heart regeneration and cardiac pathology, with a hands-on session focused on atrioventricular septal defects. Of historical interest for the ESC working group and JCDD, Etienne-Louis Arthur Fallot (1850–1911) was Professor of Anatomy at the Hôpital de la Conception in Marseille when he published his description of the tetralogy of cardiac anomalies that define "la maladie bleue" in 1888.

Manuscripts should be submitted to JCDD before 31 December, 2018 for issue publication in spring 2019.

Dr. Stephane Zaffran
Dr. Robert G. Kelly
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 papers will be 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 quarterly 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 1000 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.

Published Papers (2 papers)

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Research

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Open AccessFeature PaperArticle
Inhibition of let-7c Regulates Cardiac Regeneration after Cryoinjury in Adult Zebrafish
J. Cardiovasc. Dev. Dis. 2019, 6(2), 16; https://doi.org/10.3390/jcdd6020016
Received: 31 January 2019 / Revised: 30 March 2019 / Accepted: 1 April 2019 / Published: 4 April 2019
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Abstract
The let-7c family of micro-RNAs (miRNAs) is expressed during embryonic development and plays an important role in cell differentiation. We have investigated the role of let-7c in heart regeneration after injury in adult zebrafish. let-7c antagomir or scramble injections were given at one [...] Read more.
The let-7c family of micro-RNAs (miRNAs) is expressed during embryonic development and plays an important role in cell differentiation. We have investigated the role of let-7c in heart regeneration after injury in adult zebrafish. let-7c antagomir or scramble injections were given at one day after cryoinjury (1 dpi). Tissue samples were collected at 7 dpi, 14 dpi and 28 dpi and cardiac function was assessed before cryoinjury, 1 dpi, 7 dpi, 14 dpi and 28 dpi. Inhibition of let-7c increased the rate of fibrinolysis, increased the number of proliferating cell nuclear antigen (PCNA) positive cardiomyocytes at 7 dpi and increased the expression of the epicardial marker raldh2 at 7 dpi. Additionally, cardiac function measured with echocardiography recovered slightly more rapidly after inhibition of let-7c. These results reveal a beneficial role of let-7c inhibition in adult zebrafish heart regeneration. Full article
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Review

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Open AccessReview
Hypoplastic Left Heart Syndrome: A New Paradigm for an Old Disease?
J. Cardiovasc. Dev. Dis. 2019, 6(1), 10; https://doi.org/10.3390/jcdd6010010
Received: 24 January 2019 / Revised: 12 February 2019 / Accepted: 19 February 2019 / Published: 23 February 2019
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Abstract
Hypoplastic left heart syndrome occurs in up to 3% of all infants born with congenital heart disease and is a leading cause of death in this population. Although there is strong evidence for a genetic component, a specific genetic cause is only known [...] Read more.
Hypoplastic left heart syndrome occurs in up to 3% of all infants born with congenital heart disease and is a leading cause of death in this population. Although there is strong evidence for a genetic component, a specific genetic cause is only known in a small subset of patients, consistent with a multifactorial etiology for the syndrome. There is controversy surrounding the mechanisms underlying the syndrome, which is likely due, in part, to the phenotypic variability of the disease. The most commonly held view is that the “decreased” growth of the left ventricle is due to a decreased flow during a critical period of ventricular development. Research has also been hindered by what has been, up until now, a lack of genetically engineered animal models that faithfully reproduce the human disease. There is a growing body of evidence, nonetheless, indicating that the hypoplasia of the left ventricle is due to a primary defect in ventricular development. In this review, we discuss the evidence demonstrating that, at least for a subset of cases, the chamber hypoplasia is the consequence of hyperplasia of the contained cardiomyocytes. In this regard, hypoplastic left heart syndrome could be viewed as a neonatal form of cardiomyopathy. We also discuss the role of the endocardium in the development of the ventricular hypoplasia, which may provide a mechanistic basis for how impaired flow to the developing ventricle leads to the anatomical changes seen in the syndrome. Full article
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J. Cardiovasc. Dev. Dis. EISSN 2308-3425 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
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