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Cells
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Advances in Zebrafish Cardiac Disease Models
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Advances in Zebrafish Cardiac Disease Models

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Cardiovascular System".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 4946

Special Issue Editor

Dr. Nicla Romano

E-Mail Website
Guest Editor
Dipartimento di Scienze Ecologiche e Biologiche, Università della Tuscia, 01100 Viterbo, Italy
Interests: cardiac regeneration; extracellular matrix role; cardiac hypertrophy disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Heart diseases such as hypertrophy and heart attack represent the most frequent causes of death in humans. Several research groups worldwide are currently studying the cellular, genetic and molecular mechanisms underlying the onset of cardiovascular diseases to find effective and targeted therapies for individual patients. In this context, studies in alternative animal models, IPSC and organoids can be conducted to investigate repair strategies for human heart tissues. Furthermore, such studies can teach us which repair mechanisms or drugs are potentially effective. Even stochastic mechanisms that underlie the phenotypic differentiation/regeneration of cardiomyocytes could be approached by spatially resolved gene expression profiling and lineage analysis. An elective model used in the last 20 years for studying cell biology and cardiac development/repair and disease is the zebrafish (Brachidanio rerio). This Special Issue aims to expose new and emergent research in the field of cardiac regeneration and the control of pathologies by using alternative models such as the zebrafish.

Dr. Nicla Romano
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. Cells is an international peer-reviewed open access semimonthly 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

  • zebrafish
  • heart
  • cardiomyocytes
  • heart disease
  • cardiac hypertrophy
  • regenerative medicine
  • cardiac regeneration
  • translational models

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Published Papers (2 papers)

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Research

20 pages, 6678 KiB  
Article
Cfdp1 Is Essential for Cardiac Development and Function
by Panagiota Giardoglou, Panos Deloukas, George Dedoussis and Dimitris Beis
Cells 2023, 12(15), 1994; https://doi.org/10.3390/cells12151994 - 3 Aug 2023
Viewed by 1873
Abstract
Cardiovascular diseases (CVDs) are the prevalent cause of mortality worldwide. A combination of environmental and genetic effectors modulates the risk of developing them. Thus, it is vital to identify candidate genes and elucidate their role in the manifestation of the disease. Large-scale human [...] Read more.
Cardiovascular diseases (CVDs) are the prevalent cause of mortality worldwide. A combination of environmental and genetic effectors modulates the risk of developing them. Thus, it is vital to identify candidate genes and elucidate their role in the manifestation of the disease. Large-scale human studies have revealed the implication of Craniofacial Development Protein 1 (CFDP1) in Coronary Artery Disease (CAD). CFDP1 belongs to the evolutionary conserved Bucentaur (BCNT) family, and to date, its function and mechanism of action in Cardiovascular Development are still unclear. We utilized zebrafish to investigate the role of cfdp1 in the developing heart due to the high genomic homology, similarity in heart physiology, and ease of experimental manipulations. We showed that cfdp1 was expressed during development, and we tested two morpholinos and generated a cfdp1 mutant line. The cfdp1−/− embryos developed arrhythmic hearts and exhibited defective cardiac performance, which led to a lethal phenotype. Findings from both knockdown and knockout experiments showed that abrogation of cfdp1 leads to downregulation of Wnt signaling in embryonic hearts during valve development but without affecting Notch activation in this process. The cfdp1 zebrafish mutant line provides a valuable tool for unveiling the novel mechanism of regulating cardiac physiology and function. cfdp1 is essential for cardiac development, a previously unreported phenotype most likely due to early lethality in mice. The detected phenotype of bradycardia and arrhythmias is an observation with potential clinical relevance for humans carrying heterozygous CFDP1 mutations and their risk of developing CAD. Full article
(This article belongs to the Special Issue Advances in Zebrafish Cardiac Disease Models)
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17 pages, 20776 KiB  
Article
Characterization of the Zebrafish Elastin a (elnasa12235) Mutant: A New Model of Elastinopathy Leading to Heart Valve Defects
by Marie Hoareau, Naïma El Kholti, Romain Debret and Elise Lambert
Cells 2023, 12(10), 1436; https://doi.org/10.3390/cells12101436 - 21 May 2023
Cited by 1 | Viewed by 2582
Abstract
Elastic fibers are extracellular macromolecules that provide resilience and elastic recoil to elastic tissues and organs in vertebrates. They are composed of an elastin core surrounded by a mantle of fibrillin-rich microfibrils and are essentially produced during a relatively short period around birth [...] Read more.
Elastic fibers are extracellular macromolecules that provide resilience and elastic recoil to elastic tissues and organs in vertebrates. They are composed of an elastin core surrounded by a mantle of fibrillin-rich microfibrils and are essentially produced during a relatively short period around birth in mammals. Thus, elastic fibers have to resist many physical, chemical, and enzymatic constraints occurring throughout their lives, and their high stability can be attributed to the elastin protein. Various pathologies, called elastinopathies, are linked to an elastin deficiency, such as non-syndromic supravalvular aortic stenosis (SVAS), Williams–Beuren syndrome (WBS), and autosomal dominant cutis laxa (ADCL). To understand these diseases, as well as the aging process related to elastic fiber degradation, and to test potential therapeutic molecules in order to compensate for elastin impairments, different animal models have been proposed. Considering the many advantages of using zebrafish, we here characterize a zebrafish mutant for the elastin a paralog (elnasa12235) with a specific focus on the cardiovascular system and highlight premature heart valve defects at the adult stage. Full article
(This article belongs to the Special Issue Advances in Zebrafish Cardiac Disease Models)
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