Journal articles: 'Zebrafish models'

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Page, L. "Zebrafish as developmental models." Science 250, no. 4986 (December 7, 1990): 1320. http://dx.doi.org/10.1126/science.2255901.

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Daya, Alon, Rajashekar Donaka, and David Karasik. "Zebrafish models of sarcopenia." Disease Models & Mechanisms 13, no. 3 (March 1, 2020): dmm042689. http://dx.doi.org/10.1242/dmm.042689.

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Liu, Shu, and Steven D. Leach. "Zebrafish Models for Cancer." Annual Review of Pathology: Mechanisms of Disease 6, no. 1 (February 28, 2011): 71–93. http://dx.doi.org/10.1146/annurev-pathol-011110-130330.

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Golzio, C. "Zebrafish models of hypogonadisms." Annales d'Endocrinologie 79, no. 4 (September 2018): 197–98. http://dx.doi.org/10.1016/j.ando.2018.06.022.

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Bai, Qing, and Edward A. Burton. "Zebrafish models of Tauopathy." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1812, no. 3 (March 2011): 353–63. http://dx.doi.org/10.1016/j.bbadis.2010.09.004.

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Rosa, João Gabriel Santos, Carla Lima, and Monica Lopes-Ferreira. "Zebrafish Larvae Behavior Models as a Tool for Drug Screenings and Pre-Clinical Trials: A Review." International Journal of Molecular Sciences 23, no. 12 (June 14, 2022): 6647. http://dx.doi.org/10.3390/ijms23126647.

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To discover new molecules or review the biological activity and toxicity of therapeutic substances, drug development, and research relies on robust biological systems to obtain reliable results. Phenotype-based screenings can transpose the organism’s compensatory pathways by adopting multi-target strategies for treating complex diseases, and zebrafish emerged as an important model for biomedical research and drug screenings. Zebrafish’s clear correlation between neuro-anatomical and physiological features and behavior is very similar to that verified in mammals, enabling the construction of reliable and relevant experimental models for neurological disorders research. Zebrafish presents highly conserved physiological pathways that are found in higher vertebrates, including mammals, along with a robust behavioral repertoire. Moreover, it is very sensitive to pharmacological/environmental manipulations, and these behavioral phenotypes are detected in both larvae and adults. These advantages align with the 3Rs concept and qualify the zebrafish as a powerful tool for drug screenings and pre-clinical trials. This review highlights important behavioral domains studied in zebrafish larvae and their neurotransmitter systems and summarizes currently used techniques to evaluate and quantify zebrafish larvae behavior in laboratory studies.

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Wasel, Ola, and Jennifer L. Freeman. "Chemical and Genetic Zebrafish Models to Define Mechanisms of and Treatments for Dopaminergic Neurodegeneration." International Journal of Molecular Sciences 21, no. 17 (August 20, 2020): 5981. http://dx.doi.org/10.3390/ijms21175981.

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The zebrafish (Danio rerio) is routinely used in biological studies as a vertebrate model system that provides unique strengths allowing applications in studies of neurodevelopmental and neurodegenerative diseases. One specific advantage is that the neurotransmitter systems are highly conserved throughout vertebrate evolution, including between zebrafish and humans. Disruption of the dopaminergic signaling pathway is linked to multiple neurological disorders. One of the most common is Parkinson’s disease, a neurodegenerative disease associated with the loss of dopaminergic neurons, among other neuropathological characteristics. In this review, the development of the zebrafish’s dopaminergic system, focusing on genetic control of the dopaminergic system, is detailed. Second, neurotoxicant models used to study dopaminergic neuronal loss, including 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), the pesticides paraquat and rotenone, and 6-hydroxydopamine (6-OHDA), are described. Next, zebrafish genetic knockdown models of dj1, pink1, and prkn established for investigating mechanisms of Parkinson’s disease are discussed. Chemical modulators of the dopaminergic system are also highlighted to showcase the applicability of the zebrafish to identify mechanisms and treatments for neurodegenerative diseases such as Parkinson’s disease associated with the dopaminergic system.

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Pitchai, Arjun, Rajesh Kannan Rajaretinam, and Jennifer L. Freeman. "Zebrafish as an Emerging Model for Bioassay-Guided Natural Product Drug Discovery for Neurological Disorders." Medicines 6, no. 2 (May 30, 2019): 61. http://dx.doi.org/10.3390/medicines6020061.

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Most neurodegenerative diseases are currently incurable, with large social and economic impacts. Recently, there has been renewed interest in investigating natural products in the modern drug discovery paradigm as novel, bioactive small molecules. Moreover, the discovery of potential therapies for neurological disorders is challenging and involves developing optimized animal models for drug screening. In contemporary biomedicine, the growing need to develop experimental models to obtain a detailed understanding of malady conditions and to portray pioneering treatments has resulted in the application of zebrafish to close the gap between in vitro and in vivo assays. Zebrafish in pharmacogenetics and neuropharmacology are rapidly becoming a widely used organism. Brain function, dysfunction, genetic, and pharmacological modulation considerations are enhanced by both larval and adult zebrafish. Bioassay-guided identification of natural products using zebrafish presents as an attractive strategy for generating new lead compounds. Here, we see evidence that the zebrafish’s central nervous system is suitable for modeling human neurological disease and we review and evaluate natural product research using zebrafish as a vertebrate model platform to systematically identify bioactive natural products. Finally, we review recently developed zebrafish models of neurological disorders that have the potential to be applied in this field of research.

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Quelle-Regaldie, Ana, Daniel Sobrido-Cameán, Antón Barreiro-Iglesias, María Jesús Sobrido, and Laura Sánchez. "Zebrafish Models of Autosomal Dominant Ataxias." Cells 10, no. 2 (February 17, 2021): 421. http://dx.doi.org/10.3390/cells10020421.

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Hereditary dominant ataxias are a heterogeneous group of neurodegenerative conditions causing cerebellar dysfunction and characterized by progressive motor incoordination. Despite many efforts put into the study of these diseases, there are no effective treatments yet. Zebrafish models are widely used to characterize neuronal disorders due to its conserved vertebrate genetics that easily support genetic edition and their optic transparency that allows observing the intact CNS and its connections. In addition, its small size and external fertilization help to develop high throughput assays of candidate drugs. Here, we discuss the contributions of zebrafish models to the study of dominant ataxias defining phenotypes, genetic function, behavior and possible treatments. In addition, we review the zebrafish models created for X-linked repeat expansion diseases X-fragile/fragile-X tremor ataxia. Most of the models reviewed here presented neuronal damage and locomotor deficits. However, there is a generalized lack of zebrafish adult heterozygous models and there are no knock-in zebrafish models available for these diseases. The models created for dominant ataxias helped to elucidate gene function and mechanisms that cause neuronal damage. In the future, the application of new genetic edition techniques would help to develop more accurate zebrafish models of dominant ataxias.

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Lane, Sarah, Luis Alberto More, and Aarti Asnani. "Zebrafish Models of Cancer Therapy-Induced Cardiovascular Toxicity." Journal of Cardiovascular Development and Disease 8, no. 2 (January 22, 2021): 8. http://dx.doi.org/10.3390/jcdd8020008.

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Purpose of review: Both traditional and novel cancer therapies can cause cardiovascular toxicity in patients. In vivo models integrating both cardiovascular and cancer phenotypes allow for the study of on- and off-target mechanisms of toxicity arising from these agents. The zebrafish is the optimal whole organism model to screen for cardiotoxicity in a high throughput manner, while simultaneously assessing the role of cardiotoxicity pathways on the cancer therapy’s antitumor effect. Here we highlight established zebrafish models of human cardiovascular disease and cancer, the unique advantages of zebrafish to study mechanisms of cancer therapy-associated cardiovascular toxicity, and finally, important limitations to consider when using the zebrafish to study toxicity. Recent findings: Cancer therapy-associated cardiovascular toxicities range from cardiomyopathy with traditional agents to arrhythmias and thrombotic complications associated with newer targeted therapies. The zebrafish can be used to identify novel therapeutic strategies that selectively protect the heart from cancer therapy without affecting antitumor activity. Advances in genome editing technology have enabled the creation of several transgenic zebrafish lines valuable to the study of cardiovascular and cancer pathophysiology. Summary: The high degree of genetic conservation between zebrafish and humans, as well as the ability to recapitulate cardiotoxic phenotypes observed in patients with cancer, make the zebrafish an effective model to study cancer therapy-associated cardiovascular toxicity. Though this model provides several key benefits over existing in vitro and in vivo models, limitations of the zebrafish model include the early developmental stage required for most high-throughput applications.

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Hosono, Yasuyuki. "Zebrafish models for cancer research." Okayama Igakkai Zasshi (Journal of Okayama Medical Association) 134, no. 2 (August 1, 2022): 76–78. http://dx.doi.org/10.4044/joma.134.76.

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IMAMURA, SHINTARO, and MICHIAKI YAMASHITA. "II-1. Zebrafish embryonic models." NIPPON SUISAN GAKKAISHI 79, no. 5 (2013): 893. http://dx.doi.org/10.2331/suisan.79.893.

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Link, Brian A., and Ross F. Collery. "Zebrafish Models of Retinal Disease." Annual Review of Vision Science 1, no. 1 (November 24, 2015): 125–53. http://dx.doi.org/10.1146/annurev-vision-082114-035717.

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Storer, N. Y., and L. I. Zon. "Zebrafish Models of p53 Functions." Cold Spring Harbor Perspectives in Biology 2, no. 8 (May 5, 2010): a001123. http://dx.doi.org/10.1101/cshperspect.a001123.

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Shive, H. R. "Zebrafish Models for Human Cancer." Veterinary Pathology 50, no. 3 (November 30, 2012): 468–82. http://dx.doi.org/10.1177/0300985812467471.

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van Leeuwen, L. M., A. M. van der Sar, and W. Bitter. "Animal Models of Tuberculosis: Zebrafish." Cold Spring Harbor Perspectives in Medicine 5, no. 3 (November 20, 2014): a018580. http://dx.doi.org/10.1101/cshperspect.a018580.

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Walcott, Brian P., and Randall T. Peterson. "Zebrafish Models of Cerebrovascular Disease." Journal of Cerebral Blood Flow & Metabolism 34, no. 4 (February 12, 2014): 571–77. http://dx.doi.org/10.1038/jcbfm.2014.27.

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Perturbations in cerebral blood flow and abnormalities in blood vessel structure are the hallmarks of cerebrovascular disease. While there are many genetic and environmental factors that affect these entities through a heterogeneous group of disease processes, the ultimate final pathologic insult in humans is defined as a stroke, or damage to brain parenchyma. In the case of ischemic stroke, blood fails to reach its target destination whereas in hemorrhagic stroke, extravasation of blood occurs outside of the blood vessel lumen, resulting in direct damage to brain parenchyma. As these acute events can be neurologically devastating, if not fatal, development of novel therapeutics are urgently needed. The zebrafish ( Danio rerio) is an attractive model for the study of cerebrovascular disease because of its morphological and physiological similarity to human cerebral vasculature, its ability to be genetically manipulated, and its fecundity allowing for large-scale, phenotype-based screens.

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Casey, Mattie J., and Rodney A. Stewart. "Pediatric Cancer Models in Zebrafish." Trends in Cancer 6, no. 5 (May 2020): 407–18. http://dx.doi.org/10.1016/j.trecan.2020.02.006.

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Milan, David J., and Calum A. MacRae. "Zebrafish genetic models for arrhythmia." Progress in Biophysics and Molecular Biology 98, no. 2-3 (October 2008): 301–8. http://dx.doi.org/10.1016/j.pbiomolbio.2009.01.011.

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Bournele, Despina, and Dimitris Beis. "Zebrafish models of cardiovascular disease." Heart Failure Reviews 21, no. 6 (August 8, 2016): 803–13. http://dx.doi.org/10.1007/s10741-016-9579-y.

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Duncan, Kaylia M., Kusumika Mukherjee, Robert A. Cornell, and Eric C. Liao. "Zebrafish models of orofacial clefts." Developmental Dynamics 246, no. 11 (September 25, 2017): 897–914. http://dx.doi.org/10.1002/dvdy.24566.

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Allison, W. Ted. "Preface: Zebrafish Models of Neurology." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1812, no. 3 (March 2011): 333–34. http://dx.doi.org/10.1016/j.bbadis.2010.11.004.

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Salmi, Talhah M., Vicky W. T. Tan, and Andrew G. Cox. "Dissecting metabolism using zebrafish models of disease." Biochemical Society Transactions 47, no. 1 (January 30, 2019): 305–15. http://dx.doi.org/10.1042/bst20180335.

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Abstract Zebrafish (Danio rerio) are becoming an increasingly powerful model organism to study the role of metabolism in disease. Since its inception, the zebrafish model has relied on unique attributes such as the transparency of embryos, high fecundity and conservation with higher vertebrates, to perform phenotype-driven chemical and genetic screens. In this review, we describe how zebrafish have been used to reveal novel mechanisms by which metabolism regulates embryonic development, obesity, fatty liver disease and cancer. In addition, we will highlight how new approaches in advanced microscopy, transcriptomics and metabolomics using zebrafish as a model system have yielded fundamental insights into the mechanistic underpinnings of disease.

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Carradice, Duncan, and Graham J. Lieschke. "Zebrafish in hematology: sushi or science?" Blood 111, no. 7 (April 1, 2008): 3331–42. http://dx.doi.org/10.1182/blood-2007-10-052761.

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Abstract After a decade of the “modern era” of zebrafish hematology research, what have been their major contributions to hematology and what challenges does the model face? This review argues that, in hematology, zebrafish have demonstrated their suitability, are proving their utility, have supplied timely and novel discoveries, and are poised for further significant contributions. It presents an overview of the anatomy, physiology, and genetics of zebrafish hematopoiesis underpinning their use in hematology research. Whereas reverse genetic techniques enable functional studies of particular genes of interest, forward genetics remains zebrafish's particular strength. Mutants with diverse and interesting hematopoietic defects are emerging from multiple genetic screens. Some mutants model hereditary blood diseases, occasionally leading to disease genes first; others provide insights into developmental hematology. Models of malignant hematologic disorders provide tools for drug-target and pharmaceutics discovery. Numerous transgenic zebrafish with fluorescently marked blood cells enable live-cell imaging of inflammatory responses and host-pathogen interactions previously inaccessible to direct observation in vivo, revealing unexpected aspects of leukocyte behavior. Zebrafish disease models almost uniquely provide a basis for efficient whole animal chemical library screens for new therapeutics. Despite some limitations and challenges, their successes and discovery potential mean that zebrafish are here to stay in hematology research.

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Balmus, Ioana Miruna, Stefan Strungaru, Mircea Nicoara, Gabriel Plavan, Sabina Ioana Cojocaru, and Laurentiu Simion. "Preliminary Data Regarding the Effects of Oxytocin Administration on the Oxidative Stress Status of Zebrafish (Danio Rerio)." Revista de Chimie 68, no. 7 (August 15, 2017): 1640–43. http://dx.doi.org/10.37358/rc.17.7.5734.

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Zebrafish are important animal models widely used in molecular biology research. To our best knowledge, no previous study on OT effects in zebrafishes� oxidative stress status was performed. Moreover, while the zebrafish are naturally producing isotocin, the investigation of its homologue OT effects may provide consistent evidence of the possible influence of oxytocin in isotocin naturally producing teleosteens. In this way, we aimed to analyse the influence of water exposure (e.g. branchial and tegmental exposure) on two different doses of OT (33.2 ng/mL and 66.4 ng/mL) on the adult zebrafish (n = 15) oxidative stress markers. Significant differences and correlations were found in the zebrafish exposed to a higher OT concentration, although lipid peroxidation tended to decrease as the OT concentration increased. Thus, it seems that oxytocin is cross-reacting and exerts clear effect on oxidative stress status main parameters in zebrafish.

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Noel, Nicole C. L., Ian M. MacDonald, and W. Ted Allison. "Zebrafish Models of Photoreceptor Dysfunction and Degeneration." Biomolecules 11, no. 1 (January 9, 2021): 78. http://dx.doi.org/10.3390/biom11010078.

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Zebrafish are an instrumental system for the generation of photoreceptor degeneration models, which can be utilized to determine underlying causes of photoreceptor dysfunction and death, and for the analysis of potential therapeutic compounds, as well as the characterization of regenerative responses. We review the wealth of information from existing zebrafish models of photoreceptor disease, specifically as they relate to currently accepted taxonomic classes of human rod and cone disease. We also highlight that rich, detailed information can be derived from studying photoreceptor development, structure, and function, including behavioural assessments and in vivo imaging of zebrafish. Zebrafish models are available for a diversity of photoreceptor diseases, including cone dystrophies, which are challenging to recapitulate in nocturnal mammalian systems. Newly discovered models of photoreceptor disease and drusenoid deposit formation may not only provide important insights into pathogenesis of disease, but also potential therapeutic approaches. Zebrafish have already shown their use in providing pre-clinical data prior to testing genetic therapies in clinical trials, such as antisense oligonucleotide therapy for Usher syndrome.

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Noel, Nicole C. L., Ian M. MacDonald, and W. Ted Allison. "Zebrafish Models of Photoreceptor Dysfunction and Degeneration." Biomolecules 11, no. 1 (January 9, 2021): 78. http://dx.doi.org/10.3390/biom11010078.

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Zebrafish are an instrumental system for the generation of photoreceptor degeneration models, which can be utilized to determine underlying causes of photoreceptor dysfunction and death, and for the analysis of potential therapeutic compounds, as well as the characterization of regenerative responses. We review the wealth of information from existing zebrafish models of photoreceptor disease, specifically as they relate to currently accepted taxonomic classes of human rod and cone disease. We also highlight that rich, detailed information can be derived from studying photoreceptor development, structure, and function, including behavioural assessments and in vivo imaging of zebrafish. Zebrafish models are available for a diversity of photoreceptor diseases, including cone dystrophies, which are challenging to recapitulate in nocturnal mammalian systems. Newly discovered models of photoreceptor disease and drusenoid deposit formation may not only provide important insights into pathogenesis of disease, but also potential therapeutic approaches. Zebrafish have already shown their use in providing pre-clinical data prior to testing genetic therapies in clinical trials, such as antisense oligonucleotide therapy for Usher syndrome.

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Quelle-Regaldie, Ana, Daniel Sobrido-Cameán, Antón Barreiro-Iglesias, María Jesús Sobrido, and Laura Sánchez. "Zebrafish Models of Autosomal Recessive Ataxias." Cells 10, no. 4 (April 8, 2021): 836. http://dx.doi.org/10.3390/cells10040836.

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Autosomal recessive ataxias are much less well studied than autosomal dominant ataxias and there are no clearly defined systems to classify them. Autosomal recessive ataxias, which are characterized by neuronal and multisystemic features, have significant overlapping symptoms with other complex multisystemic recessive disorders. The generation of animal models of neurodegenerative disorders increases our knowledge of their cellular and molecular mechanisms and helps in the search for new therapies. Among animal models, the zebrafish, which shares 70% of its genome with humans, offer the advantages of being small in size and demonstrating rapid development, making them optimal for high throughput drug and genetic screening. Furthermore, embryo and larval transparency allows to visualize cellular processes and central nervous system development in vivo. In this review, we discuss the contributions of zebrafish models to the study of autosomal recessive ataxias characteristic phenotypes, behavior, and gene function, in addition to commenting on possible treatments found in these models. Most of the zebrafish models generated to date recapitulate the main features of recessive ataxias.

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Choi, Woorak, Hye Mi Kim, Sungho Park, Eunseop Yeom, Junsang Doh, and Sang Joon Lee. "Variation in wall shear stress in channel networks of zebrafish models." Journal of The Royal Society Interface 14, no. 127 (February 2017): 20160900. http://dx.doi.org/10.1098/rsif.2016.0900.

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Physiological functions of vascular endothelial cells (ECs) vary depending on wall shear stress (WSS) magnitude, and the functional change affects the pathologies of various cardiovascular systems. Several in vitro and in vivo models have been used to investigate the functions of ECs under different WSS conditions. However, these models have technical limitations in precisely mimicking the physiological environments of ECs and monitoring temporal variations of ECs in detail. Although zebrafish ( Danio rerio ) has several strategies to overcome these technical limitations, zebrafish cannot be used as a perfect animal model because applying various WSS conditions on blood vessels of zebrafish is difficult. This study proposes a new zebrafish model in which various WSS can be applied to the caudal vein. The WSS magnitude is controlled by blocking some parts of blood-vessel networks. The accuracy and reproducibility of the proposed method are validated using an equivalent circuit model of blood vessels in zebrafish. The proposed method is applied to lipopolysaccharide (LPS)-stimulated zebrafish as a typical application. The proposed zebrafish model can be used as an in vivo animal model to investigate the relationship between WSS and EC physiology or WSS-induced cardiovascular diseases.

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Basheer, Faiza, Poshmaal Dhar, and Rasika M. Samarasinghe. "Zebrafish Models of Paediatric Brain Tumours." International Journal of Molecular Sciences 23, no. 17 (August 31, 2022): 9920. http://dx.doi.org/10.3390/ijms23179920.

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Paediatric brain cancer is the second most common childhood cancer and is the leading cause of cancer-related deaths in children. Despite significant advancements in the treatment modalities and improvements in the 5-year survival rate, it leaves long-term therapy-associated side effects in paediatric patients. Addressing these impairments demands further understanding of the molecularity and heterogeneity of these brain tumours, which can be demonstrated using different animal models of paediatric brain cancer. Here we review the use of zebrafish as potential in vivo models for paediatric brain tumour modelling, as well as catalogue the currently available zebrafish models used to study paediatric brain cancer pathophysiology, and discuss key findings, the unique attributes that these models add, current challenges and therapeutic significance.

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Kolesnikova, Tatiana O., Konstantin A. Demin, Fabiano V. Costa, Konstantin N. Zabegalov, Murilo S. de Abreu, Elena V. Gerasimova, and Allan V. Kalueff. "Towards Zebrafish Models of CNS Channelopathies." International Journal of Molecular Sciences 23, no. 22 (November 12, 2022): 13979. http://dx.doi.org/10.3390/ijms232213979.

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Channelopathies are a large group of systemic disorders whose pathogenesis is associated with dysfunctional ion channels. Aberrant transmembrane transport of K+, Na+, Ca2+ and Cl− by these channels in the brain induces central nervous system (CNS) channelopathies, most commonly including epilepsy, but also migraine, as well as various movement and psychiatric disorders. Animal models are a useful tool for studying pathogenesis of a wide range of brain disorders, including channelopathies. Complementing multiple well-established rodent models, the zebrafish (Danio rerio) has become a popular translational model organism for neurobiology, psychopharmacology and toxicology research, and for probing mechanisms underlying CNS pathogenesis. Here, we discuss current prospects and challenges of developing genetic, pharmacological and other experimental models of major CNS channelopathies based on zebrafish.

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Lee, Wen-Chih, Ming-Der Lin, Wen-Ying Lin, KameshwaraKumar Dharini, Cheng-Huan Peng, Chung-Yen Lin, and Kuang-Ting Yeh. "Zebrafish models for glucocorticoid-induced osteoporosis." Tzu Chi Medical Journal 34, no. 4 (2022): 373. http://dx.doi.org/10.4103/tcmj.tcmj_80_22.

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Kawahara, Genri. "Therapeutic drug screening with zebrafish models." Folia Pharmacologica Japonica 156, no. 6 (2021): 355–58. http://dx.doi.org/10.1254/fpj.21060.

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Hsu, Hwei-Jan, Nai-Chi Hsu, Meng-Chun Hu, and Bon-Chu Chung. "Steroidogenesis in zebrafish and mouse models." Molecular and Cellular Endocrinology 248, no. 1-2 (March 2006): 160–63. http://dx.doi.org/10.1016/j.mce.2005.10.011.

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Bandmann, Oliver, and Edward A. Burton. "Genetic zebrafish models of neurodegenerative diseases." Neurobiology of Disease 40, no. 1 (October 2010): 58–65. http://dx.doi.org/10.1016/j.nbd.2010.05.017.

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Gawel, Kinga, Melanie Langlois, Teresa Martins, Wietske van der Ent, Ettore Tiraboschi, Maxime Jacmin, Alexander D. Crawford, and Camila V. Esguerra. "Seizing the moment: Zebrafish epilepsy models." Neuroscience & Biobehavioral Reviews 116 (September 2020): 1–20. http://dx.doi.org/10.1016/j.neubiorev.2020.06.010.

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Sager, Jonathan J., Qing Bai, and Edward A. Burton. "Transgenic zebrafish models of neurodegenerative diseases." Brain Structure and Function 214, no. 2-3 (February 17, 2010): 285–302. http://dx.doi.org/10.1007/s00429-009-0237-1.

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Meshalkina, Daria A., Marina N. Kizlyk, Elana V. Kysil, Adam D. Collier, David J. Echevarria, Murilo S. Abreu, Leonardo J. G. Barcellos, et al. "Zebrafish models of autism spectrum disorder." Experimental Neurology 299 (January 2018): 207–16. http://dx.doi.org/10.1016/j.expneurol.2017.02.004.

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Gaudenzi, Germano, and Giovanni Vitale. "Transplantable zebrafish models of neuroendocrine tumors." Annales d'Endocrinologie 80, no. 3 (June 2019): 149–52. http://dx.doi.org/10.1016/j.ando.2019.04.013.

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Fonseka, Trehani M., Xiao-Yan Wen, Jane A. Foster, and Sidney H. Kennedy. "Zebrafish models of major depressive disorders." Journal of Neuroscience Research 94, no. 1 (October 9, 2015): 3–14. http://dx.doi.org/10.1002/jnr.23639.

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Fish, Richard J., Corinne Di Sanza, and Marguerite Neerman-Arbez. "Targeted mutation of zebrafish fga models human congenital afibrinogenemia." Blood 123, no. 14 (April 3, 2014): 2278–81. http://dx.doi.org/10.1182/blood-2013-12-547182.

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Key Points Targeted mutation of a zebrafish fibrinogen gene leads to a bleeding phenotype, analogous to human congenital afibrinogenemia. This first heritable coagulopathy model validates the use of zebrafish for thrombosis and hemostasis research.

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Crouzier, Lucie, Elodie M. Richard, Jo Sourbron, Lieven Lagae, Tangui Maurice, and Benjamin Delprat. "Use of Zebrafish Models to Boost Research in Rare Genetic Diseases." International Journal of Molecular Sciences 22, no. 24 (December 12, 2021): 13356. http://dx.doi.org/10.3390/ijms222413356.

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Rare genetic diseases are a group of pathologies with often unmet clinical needs. Even if rare by a single genetic disease (from 1/2000 to 1/more than 1,000,000), the total number of patients concerned account for approximatively 400 million peoples worldwide. Finding treatments remains challenging due to the complexity of these diseases, the small number of patients and the challenge in conducting clinical trials. Therefore, innovative preclinical research strategies are required. The zebrafish has emerged as a powerful animal model for investigating rare diseases. Zebrafish combines conserved vertebrate characteristics with high rate of breeding, limited housing requirements and low costs. More than 84% of human genes responsible for diseases present an orthologue, suggesting that the majority of genetic diseases could be modelized in zebrafish. In this review, we emphasize the unique advantages of zebrafish models over other in vivo models, particularly underlining the high throughput phenotypic capacity for therapeutic screening. We briefly introduce how the generation of zebrafish transgenic lines by gene-modulating technologies can be used to model rare genetic diseases. Then, we describe how zebrafish could be phenotyped using state-of-the-art technologies. Two prototypic examples of rare diseases illustrate how zebrafish models could play a critical role in deciphering the underlying mechanisms of rare genetic diseases and their use to identify innovative therapeutic solutions.

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Elmonem, Mohamed, Sante Berlingerio, Lambertus van den Heuvel, Peter de Witte, Martin Lowe, and Elena Levtchenko. "Genetic Renal Diseases: The Emerging Role of Zebrafish Models." Cells 7, no. 9 (September 1, 2018): 130. http://dx.doi.org/10.3390/cells7090130.

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The structural and functional similarity of the larval zebrafish pronephros to the human nephron, together with the recent development of easier and more precise techniques to manipulate the zebrafish genome have motivated many researchers to model human renal diseases in the zebrafish. Over the last few years, great advances have been made, not only in the modeling techniques of genetic diseases in the zebrafish, but also in how to validate and exploit these models, crossing the bridge towards more informative explanations of disease pathophysiology and better designed therapeutic interventions in a cost-effective in vivo system. Here, we review the significant progress in these areas giving special attention to the renal phenotype evaluation techniques. We further discuss the future applications of such models, particularly their role in revealing new genetic diseases of the kidney and their potential use in personalized medicine.

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Ichii, Shogo, Izumi Matsuoka, Fumiyoshi Okazaki, and Yasuhito Shimada. "Zebrafish Models for Skeletal Muscle Senescence: Lessons from Cell Cultures and Rodent Models." Molecules 27, no. 23 (December 6, 2022): 8625. http://dx.doi.org/10.3390/molecules27238625.

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Human life expectancy has markedly increased over the past hundred years. Consequently, the percentage of elderly people is increasing. Aging and sarcopenic changes in skeletal muscles not only reduce locomotor activities in elderly people but also increase the chance of trauma, such as bone fractures, and the incidence of other diseases, such as metabolic syndrome, due to reduced physical activity. Exercise therapy is currently the only treatment and prevention approach for skeletal muscle aging. In this review, we aimed to summarize the strategies for modeling skeletal muscle senescence in cell cultures and rodents and provide future perspectives based on zebrafish models. In cell cultures, in addition to myoblast proliferation and myotube differentiation, senescence induction into differentiated myotubes is also promising. In rodents, several models have been reported that reflect the skeletal muscle aging phenotype or parts of it, including the accelerated aging models. Although there are fewer models of skeletal muscle aging in zebrafish than in mice, various models have been reported in recent years with the development of CRISPR/Cas9 technology, and further advancements in the field using zebrafish models are expected in the future.

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Wei, Wei, Shue Wang, Xue-Jun Zhang, Jiu-Xun Zhang, Zheng-Wang Chen, Jia-Ying Huang, and Ye-Wang Zhang. "The Effects of Mung Bean Peptide and Its’ Complexes on the Treatment of Lead Poisoning." Journal of Food Quality 2021 (July 22, 2021): 1–7. http://dx.doi.org/10.1155/2021/2851146.

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Objective. To investigate the effects of mung bean peptide and its’ complexes on promoting lead excretion and neuroprotection of zebrafish. Methods. The lead poisoning models of zebrafish were established by lead acetate solution; the models were treated with high and low concentrations (58.3 and 175 μg/mL) of mung bean peptides, with high, medium, and low concentrations (27.8, 83.3, and 250 μg/mL) of mung bean peptide complexes, separately. The effects of the mung bean peptide complexes on the lead content, axonal fluorescence intensity, and peripheral motor nerve length changes were identified in the zebrafish model, and the effects of mung bean peptide and its’ complexes on zebrafish's lead excretion, axonal protection rate, and peripheral movement promotion rate of nerve regeneration were calculated. Results. The effects of high concentration of mung bean peptide (175 μg/mL) in promoting lead excretion was 29% ( p < 0.05 ), and the effect of high concentration of mung bean peptide complexes (250 μg/mL) in promoting lead excretion was 30% ( p < 0.05 ). The other concentrations of mung bean peptide and its’ complex groups did not show a noticeable lead excretion effect. The protective effects of mung bean peptide at concentrations of 58.3 and 175 μg/mL against zebrafish axonal injury were 98% and 101% ( p < 0.01 ), and the peripheral nerve regeneration promotion effects were 29% ( p > 0.05 ) and 42% ( p < 0.05 ), respectively. The protective effects of mung bean peptide complexes at concentrations of 27.8, 83.3, and 250 μg/mL against zebrafish axonal injury were 85%, 78%, and 93% ( p < 0.01 ); peripheral nerve regeneration promotion rates were 46%, 50%, and 50% ( p < 0.05 ). Conclusion. The mung bean peptide and its’ complexes can effectively promote the discharge of lead in the zebrafish lead poisoning and have protective and regeneration effects on zebrafish nerves.

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Giardoglou, Panagiota, and Dimitris Beis. "On Zebrafish Disease Models and Matters of the Heart." Biomedicines 7, no. 1 (February 28, 2019): 15. http://dx.doi.org/10.3390/biomedicines7010015.

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Coronary artery disease (CAD) is the leading form of cardiovascular disease (CVD), which is the primary cause of mortality worldwide. It is a complex disease with genetic and environmental risk factor contributions. Reports in human and mammalian models elucidate age-associated changes in cardiac function. The diverse mechanisms involved in cardiac diseases remain at the center of the research interest to identify novel strategies for prevention and therapy. Zebrafish (Danio rerio) have emerged as a valuable vertebrate model to study cardiovascular development over the last few decades. The facile genetic manipulation via forward and reverse genetic approaches combined with noninvasive, high-resolution imaging and phenotype-based screening has provided new insights to molecular pathways that orchestrate cardiac development. Zebrafish can recapitulate human cardiac pathophysiology due to gene and regulatory pathways conservation, similar heart rate and cardiac morphology and function. Thus, generations of zebrafish models utilize the functional analysis of genes involved in CAD, which are derived from large-scale human population analysis. Here, we highlight recent studies conducted on cardiovascular research focusing on the benefits of the combination of genome-wide association studies (GWAS) with functional genomic analysis in zebrafish. We further summarize the knowledge obtained from zebrafish studies that have demonstrated the architecture of the fundamental mechanisms underlying heart development, homeostasis and regeneration at the cellular and molecular levels.

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Lee, Ai Qi, Yan Li, and Zhiyuan Gong. "Inducible Liver Cancer Models in Transgenic Zebrafish to Investigate Cancer Biology." Cancers 13, no. 20 (October 14, 2021): 5148. http://dx.doi.org/10.3390/cancers13205148.

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Primary liver cancer is one of the most prevalent and deadly cancers, which incidence continues to increase while treatment response remains poor; thus, in-depth understanding of tumour events is necessary to develop more effective therapies. Animal models for liver cancer are powerful tools to reach this goal. Over the past decade, our laboratory has established multiple oncogene transgenic zebrafish lines that can be robustly induced to develop liver cancer. Histological, transcriptomic and molecular analyses validate the use of these transgenic zebrafish as experimental models for liver cancer. In this review, we provide a comprehensive summary of our findings with these inducible zebrafish liver cancer models in tumour initiation, oncogene addiction, tumour microenvironment, gender disparity, cancer cachexia, drug screening and others. Induced oncogene expression causes a rapid change of the tumour microenvironment such as inflammatory responses, increased vascularisation and rapid hepatic growth. In several models, histologically-proven carcinoma can be induced within one week of chemical inducer administration. Interestingly, the induced liver tumours show the ability to regress when the transgenic oncogene is suppressed by the withdrawal of the chemical inducer. Like human liver cancer, there is a strong bias of liver cancer severity in male zebrafish. After long-term tumour progression, liver cancer-bearing zebrafish also show symptoms of cancer cachexia such as muscle-wasting. In addition, the zebrafish models have been used to screen for anti-metastasis drugs as well as to evaluate environmental toxicants in carcinogenesis. These findings demonstrated that these inducible zebrafish liver cancer models provide rapid and convenient experimental tools for further investigation of fundamental cancer biology, with the potential for the discovery of new therapeutic approaches.

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Lee, Ai Qi, Yan Li, and Zhiyuan Gong. "Inducible Liver Cancer Models in Transgenic Zebrafish to Investigate Cancer Biology." Cancers 13, no. 20 (October 14, 2021): 5148. http://dx.doi.org/10.3390/cancers13205148.

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Primary liver cancer is one of the most prevalent and deadly cancers, which incidence continues to increase while treatment response remains poor; thus, in-depth understanding of tumour events is necessary to develop more effective therapies. Animal models for liver cancer are powerful tools to reach this goal. Over the past decade, our laboratory has established multiple oncogene transgenic zebrafish lines that can be robustly induced to develop liver cancer. Histological, transcriptomic and molecular analyses validate the use of these transgenic zebrafish as experimental models for liver cancer. In this review, we provide a comprehensive summary of our findings with these inducible zebrafish liver cancer models in tumour initiation, oncogene addiction, tumour microenvironment, gender disparity, cancer cachexia, drug screening and others. Induced oncogene expression causes a rapid change of the tumour microenvironment such as inflammatory responses, increased vascularisation and rapid hepatic growth. In several models, histologically-proven carcinoma can be induced within one week of chemical inducer administration. Interestingly, the induced liver tumours show the ability to regress when the transgenic oncogene is suppressed by the withdrawal of the chemical inducer. Like human liver cancer, there is a strong bias of liver cancer severity in male zebrafish. After long-term tumour progression, liver cancer-bearing zebrafish also show symptoms of cancer cachexia such as muscle-wasting. In addition, the zebrafish models have been used to screen for anti-metastasis drugs as well as to evaluate environmental toxicants in carcinogenesis. These findings demonstrated that these inducible zebrafish liver cancer models provide rapid and convenient experimental tools for further investigation of fundamental cancer biology, with the potential for the discovery of new therapeutic approaches.

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Santiago, Celine F., Inken G. Huttner, and Diane Fatkin. "Mechanisms of TTNtv-Related Dilated Cardiomyopathy: Insights from Zebrafish Models." Journal of Cardiovascular Development and Disease 8, no. 2 (January 25, 2021): 10. http://dx.doi.org/10.3390/jcdd8020010.

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Dilated cardiomyopathy (DCM) is a common heart muscle disorder characterized by ventricular dilation and contractile dysfunction that is associated with significant morbidity and mortality. New insights into disease mechanisms and strategies for treatment and prevention are urgently needed. Truncating variants in the TTN gene, which encodes the giant sarcomeric protein titin (TTNtv), are the most common genetic cause of DCM, but exactly how TTNtv promote cardiomyocyte dysfunction is not known. Although rodent models have been widely used to investigate titin biology, they have had limited utility for TTNtv-related DCM. In recent years, zebrafish (Danio rerio) have emerged as a powerful alternative model system for studying titin function in the healthy and diseased heart. Optically transparent embryonic zebrafish models have demonstrated key roles of titin in sarcomere assembly and cardiac development. The increasing availability of sophisticated imaging tools for assessment of heart function in adult zebrafish has revolutionized the field and opened new opportunities for modelling human genetic disorders. Genetically modified zebrafish that carry a human A-band TTNtv have now been generated and shown to spontaneously develop DCM with age. This zebrafish model will be a valuable resource for elucidating the phenotype modifying effects of genetic and environmental factors, and for exploring new drug therapies.

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Tonon, Federica, Rossella Farra, Cristina Zennaro, Gabriele Pozzato, Nhung Truong, Salvatore Parisi, Flavio Rizzolio, et al. "Xenograft Zebrafish Models for the Development of Novel Anti-Hepatocellular Carcinoma Molecules." Pharmaceuticals 14, no. 8 (August 16, 2021): 803. http://dx.doi.org/10.3390/ph14080803.

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Hepatocellular carcinoma (HCC) is the sixth most common type of tumor and the second leading cause of tumor-related death worldwide. Liver cirrhosis is the most important predisposing factor for HCC. Available therapeutic approaches are not very effective, especially for advanced HCC, which is the most common form of the disease at diagnosis. New therapeutic strategies are therefore urgently needed. The use of animal models represents a relevant tool for preclinical screening of new molecules/strategies against HCC. However, several issues, including animal husbandry, limit the use of current models (rodent/pig). One animal model that has attracted the attention of the scientific community in the last 15 years is the zebrafish. This freshwater fish has several attractive features, such as short reproductive time, limited space and cost requirements for husbandry, body transparency and the fact that embryos do not show immune response to transplanted cells. To date, two different types of zebrafish models for HCC have been developed: the transgenic zebrafish and the zebrafish xenograft models. Since transgenic zebrafish models for HCC have been described elsewhere, in this review, we focus on the description of zebrafish xenograft models that have been used in the last five years to test new molecules/strategies against HCC.

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Journal articles on the topic 'Zebrafish models'

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