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JCDD
Special Issues
Cardiac Development, Regeneration and Repair
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Cardiac Development, Regeneration and Repair

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

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 14552

Special Issue Editor

Dr. Jinhu Wang

E-Mail Website
Guest Editor
Emory University School of Medicine, Atlanta, GA, USA
Interests: cardiac morphogenesis and regeneration; cardiac development; cardiac repair

Special Issue Information

Dear Colleagues, 

We are generating a Special Issue for the Journal of Cardiovascular Development and Disease focused on “Cardiac Development, Regeneration and Repair”. Endogenous regeneration mechanisms exist in adult mammals, but they possess limited regenerative abilities, leading to permanent scar formation and the development of heart failure. Numerous cell types and molecules with roles in innate heart regeneration have been previously characterized, but the details of their coordination for effective heart renewal are poorly understood. Furthermore, previous studies also demonstrated organ developmental program induction after cardiac injury in regenerative model systems. Uncovering critical components of both cardiac developmental pathways and regenerative mechanisms will inspire novel therapeutic strategies to treat human heart failure. 

This Special Issue of JCDD aims to offer a comprehensive assessment of the latest updates in cardiac development, repair, and regeneration. We seek original research articles, reviews, and novel methodologies/techniques for the study of heart development and cardiac regeneration systems such as zebrafish or neonatal mammals. Prospective authors are encouraged to contact us for discussion on their submission and how it aligns with this Special Issue.

Dr. Jinhu Wang
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 morphogenesis and regeneration
  • cardiac development
  • cardiac repair

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Published Papers (6 papers)

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Research

Jump to: Review

16 pages, 8758 KiB  
Article
Tg(Δ113p53:cmyc) Transgene Upregulates glut1 Expression to Promote Zebrafish Heart Regeneration
by Zimu Tang, Kaiyuan Wang, Lijian Lo and Jun Chen
J. Cardiovasc. Dev. Dis. 2023, 10(6), 246; https://doi.org/10.3390/jcdd10060246 - 4 Jun 2023
Cited by 1 | Viewed by 1969
Abstract
The heart switches its main metabolic substrate from glucose to fatty acids shortly after birth, which is one of reasons for the loss of heart regeneration capability in adult mammals. On the contrary, metabolic shifts from oxidative phosphorylation to glucose metabolism promote cardiomyocyte [...] Read more.
The heart switches its main metabolic substrate from glucose to fatty acids shortly after birth, which is one of reasons for the loss of heart regeneration capability in adult mammals. On the contrary, metabolic shifts from oxidative phosphorylation to glucose metabolism promote cardiomyocyte (CM) proliferation after heart injury. However, how glucose transportation in CMs is regulated during heart regeneration is still not fully understood. In this report, we found that the expression of Glut1 (slc2a1) was upregulated around the injury site of zebrafish heart, accompanied by an increase in glucose uptake at the injury area. Knockout of slc2a1a impaired zebrafish heart regeneration. Our previous study has demonstrated that the expression of Δ113p53 is activated after heart injury and Δ113p53+ CMs undergo proliferation to contribute to zebrafish heart regeneration. Next, we used the Δ113p53 promoter to generate the Tg(Δ113p53:cmyc) zebrafish transgenic line. Conditional overexpression of cmyc not only significantly promoted zebrafish CM proliferation and heart regeneration but also significantly enhanced glut1 expression at the injury site. Inhibiting Glut1 diminished the increase in CM proliferation in Tg(Δ113p53:cmyc) injured hearts of zebrafish. Therefore, our results suggest that the activation of cmyc promotes heart regeneration through upregulating the expression of glut1 to speed up glucose transportation. Full article
(This article belongs to the Special Issue Cardiac Development, Regeneration and Repair)
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19 pages, 2522 KiB  
Article
Cardiomyocyte-Specific Wt1 Is Involved in Cardiac Metabolism and Response to Damage
by Sandra Díaz del Moral, Maha Benaouicha, Cristina Villa del Campo, Miguel Torres, Nicole Wagner, Kay-Dietrich Wagner, Ramón Muñoz-Chápuli and Rita Carmona
J. Cardiovasc. Dev. Dis. 2023, 10(5), 211; https://doi.org/10.3390/jcdd10050211 - 12 May 2023
Cited by 1 | Viewed by 2756 | Correction
Abstract
The Wilms tumor suppressor gene (Wt1) encodes a C2H2-type zinc-finger transcription factor that participates in transcriptional regulation, RNA metabolism, and protein–protein interactions. WT1 is involved in the development of several organs, including the kidneys and gonads, heart, spleen, adrenal glands, liver, diaphragm, and [...] Read more.
The Wilms tumor suppressor gene (Wt1) encodes a C2H2-type zinc-finger transcription factor that participates in transcriptional regulation, RNA metabolism, and protein–protein interactions. WT1 is involved in the development of several organs, including the kidneys and gonads, heart, spleen, adrenal glands, liver, diaphragm, and neuronal system. We previously provided evidence of transient WT1 expression in about 25% of cardiomyocytes of mouse embryos. Conditional deletion of Wt1 in the cardiac troponin T lineage caused abnormal cardiac development. A low expression of WT1 has also been reported in adult cardiomyocytes. Therefore, we aimed to explore its function in cardiac homeostasis and in the response to pharmacologically induced damage. Silencing of Wt1 in cultured neonatal murine cardiomyocytes provoked alterations in mitochondrial membrane potential and changes in the expression of genes related to calcium homeostasis. Ablation of WT1 in adult cardiomyocytes by crossing αMHCMerCreMer mice with homozygous WT1-floxed mice induced hypertrophy, interstitial fibrosis, altered metabolism, and mitochondrial dysfunction. In addition, conditional deletion of WT1 in adult cardiomyocytes increased doxorubicin-induced damage. These findings suggest a novel role of WT1 in myocardial physiology and protection against damage. Full article
(This article belongs to the Special Issue Cardiac Development, Regeneration and Repair)
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15 pages, 1514 KiB  
Article
Purkinje Cardiomyocytes of the Adult Ventricular Conduction System Are Highly Diploid but Not Uniquely Regenerative
by Hirofumi Watanabe, Ge Tao, Peiheng Gan, Baylee C. Westbury, Kristie D. Cox, Kelsey Tjen, Ruolan Song, Glenn I. Fishman, Takako Makita and Henry M. Sucov
J. Cardiovasc. Dev. Dis. 2023, 10(4), 161; https://doi.org/10.3390/jcdd10040161 - 7 Apr 2023
Cited by 3 | Viewed by 2330
Abstract
Adult hearts are characterized by inefficient regeneration after injury, thus, the features that support or prevent cardiomyocyte (CM) proliferation are important to clarify. Diploid CMs are a candidate cell type that may have unique proliferative and regenerative competence, but no molecular markers are [...] Read more.
Adult hearts are characterized by inefficient regeneration after injury, thus, the features that support or prevent cardiomyocyte (CM) proliferation are important to clarify. Diploid CMs are a candidate cell type that may have unique proliferative and regenerative competence, but no molecular markers are yet known that selectively identify all or subpopulations of diploid CMs. Here, using the conduction system expression marker Cntn2-GFP and the conduction system lineage marker Etv1CreERT2, we demonstrate that Purkinje CMs that comprise the adult ventricular conduction system are disproportionately diploid (33%, vs. 4% of bulk ventricular CMs). These, however, represent only a small proportion (3%) of the total diploid CM population. Using EdU incorporation during the first postnatal week, we demonstrate that bulk diploid CMs found in the later heart enter and complete the cell cycle during the neonatal period. In contrast, a significant fraction of conduction CMs persist as diploid cells from fetal life and avoid neonatal cell cycle activity. Despite their high degree of diploidy, the Purkinje lineage had no enhanced competence to support regeneration after adult heart infarction. Full article
(This article belongs to the Special Issue Cardiac Development, Regeneration and Repair)
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Review

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29 pages, 3441 KiB  
Review
Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part II: Molecular Mechanisms of Cardiac Regeneration
by Juan Manuel Castillo-Casas, Sheila Caño-Carrillo, Cristina Sánchez-Fernández, Diego Franco and Estefanía Lozano-Velasco
J. Cardiovasc. Dev. Dis. 2023, 10(9), 357; https://doi.org/10.3390/jcdd10090357 - 22 Aug 2023
Cited by 3 | Viewed by 2677
Abstract
Cardiovascular diseases are the leading cause of death worldwide, among which ischemic heart disease is the most representative. Myocardial infarction results from occlusion of a coronary artery, which leads to an insufficient blood supply to the myocardium. As it is well known, the [...] Read more.
Cardiovascular diseases are the leading cause of death worldwide, among which ischemic heart disease is the most representative. Myocardial infarction results from occlusion of a coronary artery, which leads to an insufficient blood supply to the myocardium. As it is well known, the massive loss of cardiomyocytes cannot be solved due the limited regenerative ability of the adult mammalian hearts. In contrast, some lower vertebrate species can regenerate the heart after an injury; their study has disclosed some of the involved cell types, molecular mechanisms and signaling pathways during the regenerative process. In this ‘two parts’ review, we discuss the current state-of-the-art of the main response to achieve heart regeneration, where several processes are involved and essential for cardiac regeneration. Full article
(This article belongs to the Special Issue Cardiac Development, Regeneration and Repair)
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10 pages, 715 KiB  
Review
Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart—Part I: Experimental Injury Models to Study Cardiac Regeneration
by Juan Manuel Castillo-Casas, Sheila Caño-Carrillo, Cristina Sánchez-Fernández, Diego Franco and Estefanía Lozano-Velasco
J. Cardiovasc. Dev. Dis. 2023, 10(8), 325; https://doi.org/10.3390/jcdd10080325 - 31 Jul 2023
Cited by 2 | Viewed by 2014
Abstract
Cardiovascular diseases are the leading cause of death worldwide, among which, ischemic heart disease is the most prevalent. Myocardial infarction results from occlusion of a coronary artery, which leads to an insufficient blood supply to the myocardium. As is well known, the massive [...] Read more.
Cardiovascular diseases are the leading cause of death worldwide, among which, ischemic heart disease is the most prevalent. Myocardial infarction results from occlusion of a coronary artery, which leads to an insufficient blood supply to the myocardium. As is well known, the massive loss of cardiomyocytes cannot be solved due the limited regenerative ability of the adult mammalian heart. In contrast, some lower vertebrate species can regenerate the heart after injury; their study has disclosed some of the involved cell types, molecular mechanisms and signaling pathways during the regenerative process. In this two-part review, we discuss the current state of the principal response in heart regeneration, where several involved processes are essential for full cardiac function in recovery. Full article
(This article belongs to the Special Issue Cardiac Development, Regeneration and Repair)
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14 pages, 3333 KiB  
Review
Developmental Aspects of Cardiac Adaptation to Increased Workload
by Bohuslav Ostadal, Frantisek Kolar, Ivana Ostadalova, David Sedmera, Veronika Olejnickova, Marketa Hlavackova and Petra Alanova
J. Cardiovasc. Dev. Dis. 2023, 10(5), 205; https://doi.org/10.3390/jcdd10050205 - 10 May 2023
Viewed by 2104
Abstract
The heart is capable of extensive adaptive growth in response to the demands of the body. When the heart is confronted with an increased workload over a prolonged period, it tends to cope with the situation by increasing its muscle mass. The adaptive [...] Read more.
The heart is capable of extensive adaptive growth in response to the demands of the body. When the heart is confronted with an increased workload over a prolonged period, it tends to cope with the situation by increasing its muscle mass. The adaptive growth response of the cardiac muscle changes significantly during phylogenetic and ontogenetic development. Cold-blooded animals maintain the ability for cardiomyocyte proliferation even in adults. On the other hand, the extent of proliferation during ontogenetic development in warm-blooded species shows significant temporal limitations: whereas fetal and neonatal cardiac myocytes express proliferative potential (hyperplasia), after birth proliferation declines and the heart grows almost exclusively by hypertrophy. It is, therefore, understandable that the regulation of the cardiac growth response to the increased workload also differs significantly during development. The pressure overload (aortic constriction) induced in animals before the switch from hyperplastic to hypertrophic growth leads to a specific type of left ventricular hypertrophy which, in contrast with the same stimulus applied in adulthood, is characterized by hyperplasia of cardiomyocytes, capillary angiogenesis and biogenesis of collagenous structures, proportional to the growth of myocytes. These studies suggest that timing may be of crucial importance in neonatal cardiac interventions in humans: early definitive repairs of selected congenital heart disease may be more beneficial for the long-term results of surgical treatment. Full article
(This article belongs to the Special Issue Cardiac Development, Regeneration and Repair)
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