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JCDD
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Gene Regulation in Cardiac Development and Disease
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Gene Regulation in Cardiac Development and Disease

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 10337

Special Issue Editor

Dr. Francisco J. Naya

E-Mail Website
Guest Editor
1. Program in Molecular Biology, Cell Biology and Biochemistry, Boston University, Boston, MA 02215, USA
2. Department of Biology, Boston University, Boston, MA 02215, USA
Interests: cardiac development and disease; gene regulation; transcription factors; noncoding RNAs; mouse developmental biology

Special Issue Information

Dear Colleagues,

Formation of the heart is among the most dynamic and fascinating processes in animal development. A multitude of cardiac cell types are specified from distinct mesodermal progenitors and assembled with such anatomical precision that ensures this vital contractile organ will fulfill its ultimate role: the lifelong uninterrupted pumping of blood. Despite the wealth of information that has accumulated over several decades, new and unexpected regulatory mechanisms that drive cardiac lineage progression and morphogenesis continue to emerge. A better understanding of the gene regulatory networks in cardiac development is a prerequisite for the development of therapies to treat a range of heart diseases from congenital abnormalities to adult cardiomyopathies.

This Special Issue of JCDD focused on “Gene Regulation in Cardiac Development and Disease” provides a multi-factorial and systems-level view of gene regulation including transcription factors, chromatin modifying enzymes, and noncoding RNAs. The development of sophisticated analytical tools used to investigate cardiac development at the cellular and genome-wide levels has revealed a far more nuanced view of mechanisms in cardiac development. We hope to highlight cutting-edge techniques such as single cell transcriptomics and large-scale genomic and epigenomic platforms that are employed to dissect the complex and inter-connected gene regulatory networks involved in the formation of the heart from various model systems.

Dr. Francisco J. Naya
Guest Editor

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

  • cardiac development
  • gene regulation
  • transcription factor
  • chromatin
  • epigenetics
  • noncoding RNA
  • transcriptomics
  • genomics

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Published Papers (4 papers)

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Review

13 pages, 1060 KiB  
Review
Drosophila as a Model to Understand Second Heart Field Development
by Cayleen Bileckyj, Brenna Blotz and Richard M. Cripps
J. Cardiovasc. Dev. Dis. 2023, 10(12), 494; https://doi.org/10.3390/jcdd10120494 - 12 Dec 2023
Cited by 2 | Viewed by 1766
Abstract
The genetic model system Drosophila has contributed fundamentally to our understanding of mammalian heart specification, development, and congenital heart disease. The relatively simple Drosophila heart is a linear muscular tube that is specified and develops in the embryo and persists throughout the life [...] Read more.
The genetic model system Drosophila has contributed fundamentally to our understanding of mammalian heart specification, development, and congenital heart disease. The relatively simple Drosophila heart is a linear muscular tube that is specified and develops in the embryo and persists throughout the life of the animal. It functions at all stages to circulate hemolymph within the open circulatory system of the body. During Drosophila metamorphosis, the cardiac tube is remodeled, and a new layer of muscle fibers spreads over the ventral surface of the heart to form the ventral longitudinal muscles. The formation of these fibers depends critically upon genes known to be necessary for mammalian second heart field (SHF) formation. Here, we review the prior contributions of the Drosophila system to the understanding of heart development and disease, discuss the importance of the SHF to mammalian heart development and disease, and then discuss how the ventral longitudinal adult cardiac muscles can serve as a novel model for understanding SHF development and disease. Full article
(This article belongs to the Special Issue Gene Regulation in Cardiac Development and Disease)
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13 pages, 1643 KiB  
Review
Massively Parallel Reporter Assays for High-Throughput In Vivo Analysis of Cis-Regulatory Elements
by Yanjiang Zheng and Nathan J. VanDusen
J. Cardiovasc. Dev. Dis. 2023, 10(4), 144; https://doi.org/10.3390/jcdd10040144 - 29 Mar 2023
Cited by 5 | Viewed by 3517
Abstract
The rapid improvement of descriptive genomic technologies has fueled a dramatic increase in hypothesized connections between cardiovascular gene expression and phenotypes. However, in vivo testing of these hypotheses has predominantly been relegated to slow, expensive, and linear generation of genetically modified mice. In [...] Read more.
The rapid improvement of descriptive genomic technologies has fueled a dramatic increase in hypothesized connections between cardiovascular gene expression and phenotypes. However, in vivo testing of these hypotheses has predominantly been relegated to slow, expensive, and linear generation of genetically modified mice. In the study of genomic cis-regulatory elements, generation of mice featuring transgenic reporters or cis-regulatory element knockout remains the standard approach. While the data obtained is of high quality, the approach is insufficient to keep pace with candidate identification and therefore results in biases introduced during the selection of candidates for validation. However, recent advances across a range of disciplines are converging to enable functional genomic assays that can be conducted in a high-throughput manner. Here, we review one such method, massively parallel reporter assays (MPRAs), in which the activities of thousands of candidate genomic regulatory elements are simultaneously assessed via the next-generation sequencing of a barcoded reporter transcript. We discuss best practices for MPRA design and use, with a focus on practical considerations, and review how this emerging technology has been successfully deployed in vivo. Finally, we discuss how MPRAs are likely to evolve and be used in future cardiovascular research. Full article
(This article belongs to the Special Issue Gene Regulation in Cardiac Development and Disease)
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38 pages, 1855 KiB  
Review
The Role of ncRNAs in Cardiac Infarction and Regeneration
by Sheila Caño-Carrillo, Estefanía Lozano-Velasco, Juan Manuel Castillo-Casas, Cristina Sánchez-Fernández and Diego Franco
J. Cardiovasc. Dev. Dis. 2023, 10(3), 123; https://doi.org/10.3390/jcdd10030123 - 15 Mar 2023
Cited by 6 | Viewed by 1990
Abstract
Myocardial infarction is the most prevalent cardiovascular disease worldwide, and it is defined as cardiomyocyte cell death due to a lack of oxygen supply. Such a temporary absence of oxygen supply, or ischemia, leads to extensive cardiomyocyte cell death in the affected myocardium. [...] Read more.
Myocardial infarction is the most prevalent cardiovascular disease worldwide, and it is defined as cardiomyocyte cell death due to a lack of oxygen supply. Such a temporary absence of oxygen supply, or ischemia, leads to extensive cardiomyocyte cell death in the affected myocardium. Notably, reactive oxygen species are generated during the reperfusion process, driving a novel wave of cell death. Consequently, the inflammatory process starts, followed by fibrotic scar formation. Limiting inflammation and resolving the fibrotic scar are essential biological processes with respect to providing a favorable environment for cardiac regeneration that is only achieved in a limited number of species. Distinct inductive signals and transcriptional regulatory factors are key components that modulate cardiac injury and regeneration. Over the last decade, the impact of non-coding RNAs has begun to be addressed in many cellular and pathological processes including myocardial infarction and regeneration. Herein, we provide a state-of-the-art review of the current functional role of diverse non-coding RNAs, particularly microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), in different biological processes involved in cardiac injury as well as in distinct experimental models of cardiac regeneration. Full article
(This article belongs to the Special Issue Gene Regulation in Cardiac Development and Disease)
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16 pages, 1961 KiB  
Review
Molecular Mechanism Underlying Role of the XBP1s in Cardiovascular Diseases
by Shu Liu, Hong Ding, Yongnan Li and Xiaowei Zhang
J. Cardiovasc. Dev. Dis. 2022, 9(12), 459; https://doi.org/10.3390/jcdd9120459 - 14 Dec 2022
Cited by 3 | Viewed by 2439
Abstract
Spliced X-box binding protein-1 (XBP1s) is a protein that belongs to the cAMP-response element-binding (CREB)/activating transcription factor (ATF) b-ZIP family with a basic-region leucine zipper (bZIP). There is mounting evidence to suggest that XBP1s performs a critical function in a range of different [...] Read more.
Spliced X-box binding protein-1 (XBP1s) is a protein that belongs to the cAMP-response element-binding (CREB)/activating transcription factor (ATF) b-ZIP family with a basic-region leucine zipper (bZIP). There is mounting evidence to suggest that XBP1s performs a critical function in a range of different cardiovascular diseases (CVDs), indicating that it is necessary to gain a comprehensive knowledge of the processes involved in XBP1s in various disorders to make progress in research and clinical therapy. In this research, we provide a summary of the functions that XBP1s performs in the onset and advancement of CVDs such as atherosclerosis, hypertension, cardiac hypertrophy, and heart failure. Furthermore, we discuss XBP1s as a novel therapeutic target for CVDs. Full article
(This article belongs to the Special Issue Gene Regulation in Cardiac Development and Disease)
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