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Zebrafish: A Model Organism for Human Health and Disease
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Zebrafish: A Model Organism for Human Health and Disease

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: 20 March 2025 | Viewed by 9908

Special Issue Editor

Dr. Jyotshna Kanungo

E-Mail Website
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

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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

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Published Papers (7 papers)

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Research

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18 pages, 3811 KiB  
Article
Deletion of Slc1a4 Suppresses Single Mauthner Cell Axon Regeneration In Vivo through Growth-Associated Protein 43
by Keqiang Li, Dinggang Fan, Junhui Zhou, Ziang Zhao, Along Han, Zheng Song, Xiahui Tang and Bing Hu
Int. J. Mol. Sci. 2024, 25(20), 10950; https://doi.org/10.3390/ijms252010950 - 11 Oct 2024
Viewed by 741
Abstract
Spinal cord injury (SCI) is a debilitating central nervous system (CNS) disorder that leads to significant motor and sensory impairments. Given the limited regenerative capacity of adult mammalian neurons, this study presents an innovative strategy to enhance axonal regeneration and functional recovery by [...] Read more.
Spinal cord injury (SCI) is a debilitating central nervous system (CNS) disorder that leads to significant motor and sensory impairments. Given the limited regenerative capacity of adult mammalian neurons, this study presents an innovative strategy to enhance axonal regeneration and functional recovery by identifying a novel factor that markedly promotes axonal regeneration. Employing a zebrafish model with targeted single axon injury in Mauthner cells (M-cells) and utilizing the Tg (Tol056: EGFP) transgenic line for in vivo monitoring, we investigate the intrinsic mechanisms underlying axonal regeneration. This research specifically examines the role of amino acid transport, emphasizing the role of the solute carrier 1A4 amino acid transporter in axonal regeneration. Our findings demonstrate that Slc1a4 overexpression significantly enhances axonal regeneration in M-cells, whereas Slc1a4 deficiency impedes this process, which is concomitant with the downregulation of the P53/Gap43 signaling pathway. By elucidating the fundamental role of Slc1a4 in axonal regeneration and uncovering its underlying mechanisms, this study thus provides novel insights into therapeutic strategies for SCI. Full article
(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)
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12 pages, 2256 KiB  
Article
Short- and Long-Term Neurobehavioral Effects of Developmental Exposure to Valproic Acid in Zebrafish
by Marina Ricarte, Niki Tagkalidou, Marina Bellot, Juliette Bedrossiantz, Eva Prats, Cristian Gomez-Canela, Natalia Garcia-Reyero and Demetrio Raldúa
Int. J. Mol. Sci. 2024, 25(14), 7688; https://doi.org/10.3390/ijms25147688 - 13 Jul 2024
Viewed by 1286
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social interaction and communication, anxiety, hyperactivity, and interest restricted to specific subjects. In addition to the genetic factors, multiple environmental factors have been related to the development of ASD. Animal models [...] Read more.
Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impairments in social interaction and communication, anxiety, hyperactivity, and interest restricted to specific subjects. In addition to the genetic factors, multiple environmental factors have been related to the development of ASD. Animal models can serve as crucial tools for understanding the complexity of ASD. In this study, a chemical model of ASD has been developed in zebrafish by exposing embryos to valproic acid (VPA) from 4 to 48 h post-fertilization, rearing them to the adult stage in fish water. For the first time, an integrative approach combining behavioral analysis and neurotransmitters profile has been used for determining the effects of early-life exposure to VPA both in the larval and adult stages. Larvae from VPA-treated embryos showed hyperactivity and decreased visual and vibrational escape responses, as well as an altered neurotransmitters profile, with increased glutamate and decreased acetylcholine and norepinephrine levels. Adults from VPA-treated embryos exhibited impaired social behavior characterized by larger shoal sizes and a decreased interest for their conspecifics. A neurotransmitter analysis revealed a significant decrease in dopamine and GABA levels in the brain. These results support the potential predictive validity of this model for ASD research. Full article
(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)
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14 pages, 4623 KiB  
Article
Characterisation of an Adult Zebrafish Model for SDHB-Associated Phaeochromocytomas and Paragangliomas
by Jasmijn B. Miltenburg, Marnix Gorissen, Inge van Outersterp, Iris Versteeg, Alex Nowak, Richard J. Rodenburg, Antonius E. van Herwaarden, Andre J. Olthaar, Benno Kusters, Catleen Conrad, Henri J. L. M. Timmers and Margo Dona
Int. J. Mol. Sci. 2024, 25(13), 7262; https://doi.org/10.3390/ijms25137262 - 1 Jul 2024
Viewed by 1026
Abstract
Phaeochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumours arising from chromaffin cells. Pathogenic variants in the gene succinate dehydrogenase subunit B (SDHB) are associated with malignancy and poor prognosis. When metastases arise, limited treatment options are available. The pathomechanism of SDHB-associated PPGL [...] Read more.
Phaeochromocytomas and paragangliomas (PPGLs) are rare neuroendocrine tumours arising from chromaffin cells. Pathogenic variants in the gene succinate dehydrogenase subunit B (SDHB) are associated with malignancy and poor prognosis. When metastases arise, limited treatment options are available. The pathomechanism of SDHB-associated PPGL remains largely unknown, and the lack of suitable models hinders therapy development. Germline heterozygous SDHB pathogenic variants predispose to developing PPGLs with a life-long penetrance of around 50%. To mimic the human disease phenotype, we characterised adult heterozygous sdhb mutant zebrafish as a potential model to study SDHB-related PPGLs. Adult sdhb mutant zebrafish did not develop an obvious tumour phenotype and were anatomically and histologically like their wild-type siblings. However, sdhb mutants showed significantly increased succinate levels, a major hallmark of SDHB-related PPGLs. While basal activity was increased during day periods in mutants, mitochondrial complex activity and catecholamine metabolite levels were not significantly different. In conclusion, we characterised an adult in vivo zebrafish model, genetically resembling human carriers. Adult heterozygous sdhb mutants mimicked their human counterparts, showing systemic elevation of succinate levels despite the absence of a tumour phenotype. This model forms a promising basis for developing a full tumour phenotype and gaining knowledge of the pathomechanism behind SDHB-related PPGLs. Full article
(This article belongs to the Special Issue Zebrafish: A Model Organism for Human Health and Disease)
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19 pages, 5110 KiB  
Article
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 1146
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), [...] Read more.
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  
Article
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 1014
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 [...] Read more.
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  
Review
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
Cited by 2 | Viewed by 1402
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 [...] Read more.
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  
Review
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
Cited by 1 | Viewed by 1477
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 [...] Read more.
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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