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Zebrafish: A Model Organism for Human Health and Disease

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 September 2024 | Viewed by 2645

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Special Issue Editor

Dr. Jyotshna Kanungo

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Guest Editor

Division of Neurotoxicology, National Center for Toxicological Research, US Food and Drug Administration, Jefferson, AR 72079, USA
Interests: neuroscience (neurodevelopment and neurodegeneration); zebrafish; developmental biology

Special Issue Information

Dear Colleagues,

Zebrafish are an attractive vertebrate model used in drug discovery. Due to their small size, external development, and transparency, zebrafish embryos are compatible with multi-well plates for high-throughput screening. Based on the availability of zebrafish genome sequences, the ease of creating transgenic and genetic mutants, and the conservation of signal transduction pathways, a variety of human diseases have been modeled using zebrafish. Moreover, biological pathways, such as physiological and molecular events, which control the development and function of most organ systems, including the cardiovascular, skeletal, nervous, digestive, and visual systems of zebrafish, are similar to those in mammals. The zebrafish reference genome published in 2013 has further accelerated the use of zebrafish in human disease modelling. In the last two decades, zebrafish have become popular in pharmaceutical and toxicological research. Consequently, several drugs have been used to treat human diseases (including tuberculosis, neuronal, and auditory disorders, as well as several types of cancer) have been identified from zebrafish screens. Such advances in this area of research have established zebrafish as an invaluable human disease model. This Special Issue aims to cover current research and provide an overview of the advances made in the area of drug discovery and disease modeling using the zebrafish model.

Dr. Jyotshna Kanungo
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.

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Keywords

zebrafish
drug discovery
high-throughput screens
genome editing/CRISPR mutants
cancer
neuronal disorders
drug toxicity
drug effect mechanisms
developmental disorders

Published Papers (4 papers)

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Research

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19 pages, 5110 KiB

Open AccessArticle

Ace Deficiency Induces Intestinal Inflammation in Zebrafish

by Mingxia Wei, Qinqing Yu, Enguang Li, Yibing Zhao, Chen Sun, Hongyan Li, Zhenhui Liu and Guangdong Ji

Int. J. Mol. Sci. 2024, 25(11), 5598; https://doi.org/10.3390/ijms25115598 - 21 May 2024

Viewed by 226

Abstract

Inflammatory bowel disease (IBD) is a nonspecific chronic inflammatory disease resulting from an immune disorder in the intestine that is prone to relapse and incurable. The understanding of the pathogenesis of IBD remains unclear. In this study, we found that ace (angiotensin-converting enzyme), expressed abundantly in the intestine, plays an important role in IBD. The deletion of ace in zebrafish caused intestinal inflammation with increased expression of the inflammatory marker genes interleukin 1 beta (il1b), matrix metallopeptidase 9 (mmp9), myeloid-specific peroxidase (mpx), leukocyte cell-derived chemotaxin-2-like (lect2l), and chemokine (C-X-C motif) ligand 8b (cxcl8b). Moreover, the secretion of mucus in the ace^−/− mutants was significantly higher than that in the wild-type zebrafish, validating the phenotype of intestinal inflammation. This was further confirmed by the IBD model constructed using dextran sodium sulfate (DSS), in which the mutant zebrafish had a higher susceptibility to enteritis. Our study reveals the role of ace in intestinal homeostasis, providing a new target for potential therapeutic interventions. Full article

(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)

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14 pages, 3400 KiB

Open AccessArticle

Mitral Cell Dendritic Morphology in the Adult Zebrafish Olfactory Bulb following Growth, Injury and Recovery

by John P. Rozofsky, Joanna M. Pozzuto and Christine A. Byrd-Jacobs

Int. J. Mol. Sci. 2024, 25(9), 5030; https://doi.org/10.3390/ijms25095030 - 5 May 2024

Viewed by 491

Abstract

The role of afferent target interactions in dendritic plasticity within the adult brain remains poorly understood. There is a paucity of data regarding the effects of deafferentation and subsequent dendritic recovery in adult brain structures. Moreover, although adult zebrafish demonstrate ongoing growth, investigations into the impact of growth on mitral cell (MC) dendritic arbor structure and complexity are lacking. Leveraging the regenerative capabilities of the zebrafish olfactory system, we conducted a comprehensive study to address these gaps. Employing an eight-week reversible deafferentation injury model followed by retrograde labeling, we observed substantial morphological alterations in MC dendrites. Our hypothesis posited that cessation of injury would facilitate recovery of MC dendritic arbor structure and complexity, potentially influenced by growth dynamics. Statistical analyses revealed significant changes in MC dendritic morphology following growth and recovery periods, indicating that MC total dendritic branch length retained significance after 8 weeks of deafferentation injury when normalized to individual fish physical characteristics. This suggests that regeneration of branch length could potentially function relatively independently of growth-related changes. These findings underscore the remarkable plasticity of adult dendritic arbor structures in a sophisticated model organism and highlight the efficacy of zebrafish as a vital implement for studying neuroregenerative processes. Full article

(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)

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Review

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24 pages, 803 KiB

Open AccessReview

Zebrafish Congenital Heart Disease Models: Opportunities and Challenges

by Dixuan Yang, Zhenjie Jian, Changfa Tang, Zhanglin Chen, Zuoqiong Zhou, Lan Zheng and Xiyang Peng

Int. J. Mol. Sci. 2024, 25(11), 5943; https://doi.org/10.3390/ijms25115943 - 29 May 2024

Viewed by 166

Abstract

Congenital heart defects (CHDs) are common human birth defects. Genetic mutations potentially cause the exhibition of various pathological phenotypes associated with CHDs, occurring alone or as part of certain syndromes. Zebrafish, a model organism with a strong molecular conservation similar to humans, is commonly used in studies on cardiovascular diseases owing to its advantageous features, such as a similarity to human electrophysiology, transparent embryos and larvae for observation, and suitability for forward and reverse genetics technology, to create various economical and easily controlled zebrafish CHD models. In this review, we outline the pros and cons of zebrafish CHD models created by genetic mutations associated with single defects and syndromes and the underlying pathogenic mechanism of CHDs discovered in these models. The challenges of zebrafish CHD models generated through gene editing are also discussed, since the cardiac phenotypes resulting from a single-candidate pathological gene mutation in zebrafish might not mirror the corresponding human phenotypes. The comprehensive review of these zebrafish CHD models will facilitate the understanding of the pathogenic mechanisms of CHDs and offer new opportunities for their treatments and intervention strategies. Full article

(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)

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15 pages, 2229 KiB

Open AccessReview

Neurogenic Effects of Inorganic Arsenic and Cdk5 Knockdown in Zebrafish Embryos: A Perspective on Modeling Autism

by Qiang Gu and Jyotshna Kanungo

Int. J. Mol. Sci. 2024, 25(6), 3459; https://doi.org/10.3390/ijms25063459 - 19 Mar 2024

Viewed by 884

Abstract

The exact mechanisms of the development of autism, a multifactorial neurological disorder, are not clear. The pathophysiology of autism is complex, and investigations at the cellular and molecular levels are ongoing to provide clarity. Mutations in specific genes have been identified as risk factors for autism. The role of heavy metals in the pathogenesis of autism is subject to many studies and remains debatable. Although no exact neuronal phenotypes have been identified linked to autistic symptoms, overproduction and reduction of specific neurons have been implicated. A growing literature on generating genetic and non-genetic models of autism aims to help with understanding mechanistic studies that can explain the complexity of the disorder. Both genetic and non-genetic methods of zebrafish have been used to model autism. For several human autism risk genes, validated zebrafish mutant models have been generated. There is growing evidence indicating a potential link between autism and inorganic arsenic exposure. We have previously shown that inorganic arsenic induces supernumerary spinal motor neurons via Sonic hedgehog (Shh) signaling pathway, and Cdk5 knockdown causes an overproduction of cranial and spinal motor neurons in zebrafish. Here, in this review, we provide a perspective on what these findings of neurogenic phenotypes mean in terms of dysregulated pathways of motor neuron development and their applicability to understanding cellular and molecular underpinnings of autism. Full article

(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)

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