ArticleThe American journal of pathology2010
Pathology of gastrointestinal organs in a porcine model of cystic fibrosis.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.
What it found
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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
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Who cites it
101 citing papers in PubMed, 159 citations in OpenAlex.
- Considerations for early life genetic therapies in cystic fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2026Review
- Advancing Gene Therapy for Pancreatitis: From Genetic Insights to Clinical Translation.Research (Washington, D.C.) · 2026Review
- ANO1: central role and clinical significance in non-neoplastic and neoplastic diseases.Frontiers in immunology · 2025Review
- Gallbladder mucoceles in dogs: a novel form of acquired CFTR dysfunction causing localized cystic fibrosis-like disease.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Acquired dysfunction of CFTR underlies cystic fibrosis-like disease of the canine gallbladder.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Genetic engineering drives the breakthrough of pig models in liver disease research.Liver research (Beijing, China) · 2024Review
- Article
- Pancreatic Crosstalk in the Disease Setting: Understanding the Impact of Exocrine Disease on Endocrine Function.Comprehensive Physiology · 2024Review
- Establishment and characterization of turtle liver organoids provides a potential model to decode their unique adaptations.Communications biology · 2024Article
- Pro-inflammatory cytokines stimulate CFTR-dependent anion secretion in pancreatic ductal epithelium.Cellular & molecular biology letters · 2024Article
- Pancreatic enzymes digest obstructive meconium from cystic fibrosis pig intestines.Frontiers in pediatrics · 2024Article
- Role of innate immunity and systemic inflammation in cystic fibrosis disease progression.Heliyon · 2023Review
- Immunohistochemical detection of MUC5AC and MUC5B mucins in ferrets.BMC research notes · 2023Article
- Cystic Fibrosis-Related Diabetes Workshop: Research Priorities Spanning Disease Pathophysiology, Diagnosis, and Outcomes.Diabetes care · 2023Review
- Cystic Fibrosis-Related Diabetes Workshop: Research Priorities Spanning Disease Pathophysiology, Diagnosis, and Outcomes.Diabetes · 2023Review
- Changes in Essential Fatty Acids and Ileal Genes Associated with Metabolizing Enzymes and Fatty Acid Transporters in Rodent Models of Cystic Fibrosis.International journal of molecular sciences · 2023Article
- Cystic fibrosis rabbits develop spontaneous hepatobiliary lesions and CF-associated liver disease (CFLD)-like phenotypes.PNAS nexus · 2023Article
- Oxidative stress and impaired insulin secretion in cystic fibrosis pig pancreas.Advances in redox research · 2022Article
- Current clinical opinion on CFTR dysfunction and patient risk of pancreatitis: diagnostic and therapeutic considerations.Expert review of gastroenterology & hepatology · 2022Article
- Use of Translational, Genetically Modified Porcine Models to Ultimately Improve Intestinal Disease Treatment.Frontiers in veterinary science · 2022Review
41 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Cystic fibrosis (CF), which is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR), is characterized by multiorgan pathology that begins early in life. To better understand the initial stages of disease, we studied the gastrointestinal pathology of CFTR-/- pigs. By studying newborns, we avoided secondary changes attributable to environmental interactions, infection, or disease progression. Lesions resembling those in humans with CF were detected in intestine, pancreas, liver, gallbladder, and cystic duct. These organs had four common features. First, disease was accelerated compared with that in humans, which could provide a strategy to discover modifying factors. Second, affected organs showed variable hyperplastic, metaplastic, and connective tissue changes, indicating that remodeling was a dynamic component of fetal life. Third, cellular inflammation was often mild to moderate and not always present, which raises new questions as to the role of cellular inflammation in early disease pathogenesis. Fourth, epithelial mucus-producing cells were often increased, producing a striking accumulation of mucus with a layered appearance and resilient structure. Thus, mucus cell hyperplasia and mucus accumulation play prominent roles in early disease. Our findings also have implications for CF lung disease, and they lay the foundation for a better understanding of CF pathogenesis.
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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.