ArticleJournal of pediatric surgery2021
Pan-enteric neuropathy and dysmotility are present in a mouse model of short-segment Hirschsprung disease and may contribute to post-pullthrough morbidity.
Article in Journal of pediatric surgery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Beyond aganglionosis: BCL-2 and Laminin signatures Elucidate Hirschsprung disease and Hirschsprung-Associated Enterocolitis pathogenesis.Pediatric research · 2026Article
- Morphological evidence suggestive of a hierarchical mode of glial cell diversification and intrinsic developmental plasticity within the murine enteric nervous system.Frontiers in neuroscience · 2025Article
- Causes and consequences: development and pathophysiology of Hirschsprung disease.World journal of pediatric surgery · 2024Review
- Depletion of muscularis macrophages ameliorates inflammation-driven dysmotility in murine colitis model.Scientific reports · 2023Article
- Endothelin signaling in development.Development (Cambridge, England) · 2023Review
- Neonatal development of intestinal neuroimmune interactions.Trends in neurosciences · 2022Review
- Review
- Article
- Reducing Underdiagnosis of Hirschsprung-Associated Enterocolitis: A Novel Scoring System.The Journal of surgical research · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
purposeHirschsprung disease (HSCR) is characterized by distal intestinal aganglionosis. While surgery is lifesaving, gastrointestinal (GI) motility disorders persist in many patients. Our objective was to determine whether enteric nervous system (ENS) abnormalities exist in the ganglionated portions of the GI tract far proximal to the aganglionic region and whether these are associated with GI dysmotility.
methodsUsing Ednrb-null mice, a model of HSCR, immunohistochemical analysis was performed to evaluate quantitatively ENS structure in proximal colon, small intestine, and stomach. Gastric emptying and intestinal transit were measured in vivo and small and large bowel contractility was assessed by spatiotemporal mapping ex vivo.
resultsProximal colon of HSCR mice had smaller ganglia and decreased neuronal fiber density, along with a marked reduction in migrating motor complexes. The distal small intestine exhibited significantly fewer ganglia and decreased neuronal fiber density, and this was associated with delayed small intestinal transit time. Finally, in the stomach of HSCR mice, enteric neuronal packing density was increased and gastric emptying was faster.
conclusionsENS abnormalities and motility defects are present throughout the ganglionated portions of the GI tract in Ednrb-deficient mice. This may explain the GI morbidity that often occurs following pull-through surgery for HSCR.
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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.