ArticleDevelopmental biology2015
Loss of cftr function leads to pancreatic destruction in larval zebrafish.
Article in Developmental biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Protein sorting and proteostasis mechanisms in CFTR-related exocrine pancreas dysfunction: A systematic narrative review.Channels (Austin, Tex.) · 2026Pooled it
- Cystic fibrosis: insights from zebrafish models.Disease models & mechanisms · 2026Review
- Phased ERK responsiveness and developmental robustness regulate teleost skin morphogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Mapping the oxidative landscape in cystic fibrosis: methodological frontiers and application.Frontiers in pharmacology · 2025Review
- Zebrafish (International journal of molecular sciences · 2024Review
- Zebrafish as an effective model for evaluating phage therapy in bacterial infections: a promising strategy against human pathogens.Antimicrobial agents and chemotherapy · 2024Review
- Decoding pancreatic endocrine cell differentiation and β cell regeneration in zebrafish.Science advances · 2023Article
- Animal models of cystic fibrosis in the era of highly effective modulator therapies.Current opinion in pharmacology · 2022Review
- Current clinical opinion on CFTR dysfunction and patient risk of pancreatitis: diagnostic and therapeutic considerations.Expert review of gastroenterology & hepatology · 2022Article
- Cystic Fibrosis and the Cells of the Airway Epithelium: What Are Ionocytes and What Do They Do?Annual review of pathology · 2022Review
- Article
- Using Zebrafish as a Disease Model to Study Fibrotic Disease.International journal of molecular sciences · 2021Review
- Article
- Zebrafish Embryo Infection Model to InvestigateFrontiers in cellular and infection microbiology · 2021Review
- Viral Vectors, Animal Models, and Cellular Targets for Gene Therapy of Cystic Fibrosis Lung Disease.Human gene therapy · 2020Review
- What Role Does CFTR Play in Development, Differentiation, Regeneration and Cancer?International journal of molecular sciences · 2020Review
- Deletion ofFrontiers in immunology · 2020Article
- Lumen Expansion Facilitates Epiblast-Primitive Endoderm Fate Specification during Mouse Blastocyst Formation.Developmental cell · 2019Article
- Activity of lumacaftor is not conserved in zebrafish Cftr bearing the major cystic fibrosis-causing mutation.FASEB bioAdvances · 2019Article
- Animal Models: Challenges and Opportunities to Determine Optimal Experimental Models of Pancreatitis and Pancreatic Cancer.Pancreas · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The development and function of many internal organs requires precisely regulated fluid secretion. A key regulator of vertebrate fluid secretion is an anion channel, the cystic fibrosis transmembrane conductance regulator (CFTR). Loss of CFTR function leads to defects in fluid transport and cystic fibrosis (CF), a complex disease characterized by a loss of fluid secretion and mucus buildup in many organs including the lungs, liver, and pancreas. Several animal models including mouse, ferret and pig have been generated to investigate the pathophysiology of CF. However, these models have limited accessibility to early processes in the development of CF and are not amenable for forward genetic or chemical screens. Here, we show that Cftr is expressed and localized to the apical membrane of the zebrafish pancreatic duct and that loss of cftr function leads to destruction of the exocrine pancreas and a cystic fibrosis phenotype that mirrors human disease. Our analyses reveal that the cftr mutant pancreas initially develops normally, then rapidly loses pancreatic tissue during larval life, reflecting pancreatic disease in CF. Altogether, we demonstrate that the cftr mutant zebrafish is a powerful new model for pancreatitis and pancreatic destruction in CF. This accessible model will allow more detailed investigation into the mechanisms that drive CF of the pancreas and facilitate development of new therapies to treat the disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.