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Cell Signaling in Heart Function, Development and Disease
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Cell Signaling in Heart Function, Development and Disease

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Basic and Translational Cardiovascular Research".

Deadline for manuscript submissions: closed (31 March 2022) | Viewed by 9351

Special Issue Editors

Prof. Dr. Michael Tsang

E-Mail Website
Guest Editor
Department of Developmental Biology, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
Interests: cardiac development; heart regeneration; disease modeling
Dr. Joshua S. Waxman

E-Mail Website
Guest Editor
Molecular Cardiovascular Biology Division and Heart Institute, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH 45229, USA
Interests: cardiac development; heart regeneration; congenital heart defects; molecular signaling pathways; transcription factors; retinoid acid signaling; zebrafish

Special Issue Information

Dear Colleagues,

Cellular signaling is a critical process in the development of the heart from its initial stages of establishing cardiac progenitors to cardiomyocyte differentiation and maturation. In addition to the contribution of endothelial, epicardial and fibroblasts cells, cellular communication is an important facet of the heart.

This Special Issue of the Journal of Cardiovascular Development and Disease will concentrate on the role of cell signaling in heart development, function and disease. We invite authors to submit original research articles, technical articles, and reviews covering all aspects of signaling factors, as well as their molecular pathways in regulating heart development, cardiac homeostasis and function, regeneration, and heart disease.

Prof. Dr. Michael Tsang
Dr. Joshua S. Waxman
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

  • cell signaling pathways
  • ligands
  • signal transduction
  • heart development
  • disease states

Published Papers (3 papers)

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Research

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17 pages, 2210 KiB  
Article
Left Ventricular Noncompaction Is Associated with Valvular Regurgitation and a Variety of Arrhythmias
by Qing Li, Lianjie Miao, Lihong Xia, Hala Y. Abdelnasser, Fang Zhang, Yangyang Lu, Anika Nusrat, Mantasha Tabassum, Juxiang Li and Mingfu Wu
J. Cardiovasc. Dev. Dis. 2022, 9(2), 49; https://doi.org/10.3390/jcdd9020049 - 2 Feb 2022
Cited by 6 | Viewed by 2325
Abstract
Left ventricular noncompaction (LVNC) is a type of cardiomyopathy characterized anatomically by prominent ventricular trabeculation and deep intertrabecular recesses. The mortality associated with LVNC ranges from 5% to 47%. The etiology of LVNC is yet to be fully understood, although decades have passed [...] Read more.
Left ventricular noncompaction (LVNC) is a type of cardiomyopathy characterized anatomically by prominent ventricular trabeculation and deep intertrabecular recesses. The mortality associated with LVNC ranges from 5% to 47%. The etiology of LVNC is yet to be fully understood, although decades have passed since its recognition as a clinical entity globally. Furthermore, critical questions, i.e., whether LVNC represents an acquired pathology or has a congenital origin and whether the reduced contractile function in LVNC patients is a cause or consequence of noncompaction, remain to be addressed. In this study, to answer some of these questions, we analyzed the clinical features of LVNC patients. Out of 9582 subjects screened for abnormal cardiac functions, 45 exhibit the characteristics of LVNC, and 1 presents right ventricular noncompaction (RVNC). We found that 40 patients show valvular regurgitation, 39 manifest reduced systolic contractions, and 46 out of the 46 present different forms of arrhythmias that are not restricted to be caused by the noncompact myocardium. This retrospective examination of LVNC patients reveals some novel findings: LVNC is associated with regurgitation in most patients and arrhythmias in all patients. The thickness ratio of the trabecular layer to compact layer negatively correlates with fractional shortening, and reduced contractility might result from LVNC. This study adds evidence to support a congenital origin of LVNC that might benefit the diagnosis and subsequent characterization of LVNC patients. Full article
(This article belongs to the Special Issue Cell Signaling in Heart Function, Development and Disease)
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Review

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24 pages, 3352 KiB  
Review
Signaling Pathways Involved in Myocardial Ischemia–Reperfusion Injury and Cardioprotection: A Systematic Review of Transcriptomic Studies in Sus scrofa
by Hector Salazar-Gonzalez, Yanet Karina Gutierrez-Mercado, Francisco Javier Munguia-Galaviz and Raquel Echavarria
J. Cardiovasc. Dev. Dis. 2022, 9(5), 132; https://doi.org/10.3390/jcdd9050132 - 26 Apr 2022
Cited by 2 | Viewed by 2830
Abstract
Myocardial damage in acute myocardial infarctions (AMI) is primarily the result of ischemia–reperfusion injury (IRI). Recognizing the timing of transcriptional events and their modulation by cardioprotective strategies is critical to address the pathophysiology of myocardial IRI. Despite the relevance of pigs for translational [...] Read more.
Myocardial damage in acute myocardial infarctions (AMI) is primarily the result of ischemia–reperfusion injury (IRI). Recognizing the timing of transcriptional events and their modulation by cardioprotective strategies is critical to address the pathophysiology of myocardial IRI. Despite the relevance of pigs for translational studies of AMI, only a few have identified how transcriptomic changes shape cellular signaling pathways in response to injury. We systematically reviewed transcriptomic studies of myocardial IRI and cardioprotection in Sus scrofa. Gene expression datasets were analyzed for significantly enriched terms using the Enrichr analysis tool, and statistically significant results (adjusted p-values of <0.05) for Signaling Pathways, Transcription Factors, Molecular Functions, and Biological Processes were compared between eligible studies to describe how these dynamic changes transform the myocardium from an injured and inflamed tissue into a scar. Then, we address how cardioprotective interventions distinctly modulate the myocardial transcriptome and discuss the implications of uncovering gene regulatory networks for cardiovascular pathologies and translational applications. Full article
(This article belongs to the Special Issue Cell Signaling in Heart Function, Development and Disease)
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13 pages, 1000 KiB  
Review
Modeling Human Heart Development and Congenital Defects Using Organoids: How Close Are We?
by Shan Jiang, Wei Feng, Cindy Chang and Guang Li
J. Cardiovasc. Dev. Dis. 2022, 9(5), 125; https://doi.org/10.3390/jcdd9050125 - 21 Apr 2022
Cited by 5 | Viewed by 3704
Abstract
The emergence of human-induced Pluripotent Stem Cells (hiPSCs) has dramatically improved our understanding of human developmental processes under normal and diseased conditions. The hiPSCs have been differentiated into various tissue-specific cells in vitro, and the advancement in three-dimensional (3D) culture has provided a [...] Read more.
The emergence of human-induced Pluripotent Stem Cells (hiPSCs) has dramatically improved our understanding of human developmental processes under normal and diseased conditions. The hiPSCs have been differentiated into various tissue-specific cells in vitro, and the advancement in three-dimensional (3D) culture has provided a possibility to generate those cells in an in vivo-like environment. Tissues with 3D structures can be generated using different approaches such as self-assembled organoids and tissue-engineering methods, such as bioprinting. We are interested in studying the self-assembled organoids differentiated from hiPSCs, as they have the potential to recapitulate the in vivo developmental process and be used to model human development and congenital defects. Organoids of tissues such as those of the intestine and brain were developed many years ago, but heart organoids were not reported until recently. In this review, we will compare the heart organoids with the in vivo hearts to understand the anatomical structures we still lack in the organoids. Specifically, we will compare the development of main heart structures, focusing on their marker genes and regulatory signaling pathways. Full article
(This article belongs to the Special Issue Cell Signaling in Heart Function, Development and Disease)
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