ArticleThe Journal of clinical investigation2021
Hirschsprung disease and more: dysregulation of ERBB2 and ERBB3.
Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 6 citations in OpenAlex.
- Postoperative Hirschsprung's associated enterocolitis (HAEC): transition zone as putative histopathological predictive factor.Journal of clinical pathology · 2025Article
- Urine miRNA signature as potential non-invasive diagnostic biomarker for Hirschsprung's disease.Frontiers in molecular neuroscience · 2024Article
- Prenatal diagnosis of fetal neurogenic megacystis associated with lethal congenital contractural syndrome 2.Case reports in perinatal medicine · 2024Article
- Unbiased characterization of the larval zebrafish enteric nervous system at a single cell transcriptomic level.iScience · 2023Article
- Adult patients with allied disorders of Hirschsprung's disease in emergency department: An 11-year retrospective study.World journal of gastrointestinal surgery · 2022Article
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Abstract
The enteric nervous system mediates reflexes independently of the brain and spinal cord and transmits signals bidirectionally between the gut and the brain. Hirschsprung disease and chronic intestinal pseudo-obstruction (CIPO) and pediatric CIPO are examples of congenital defects that impair gastrointestinal motility. In this issue of the JCI, Thuy-Linh Le et al. analyzed eight patients with defects in tissue that arose from the neural crest. The patients carried homozygous or heterozygous variants in ERBB3 or ERBB2, which encode transmembrane epidermal growth factor receptors that bind neuroregulin 1 (NRG1). Notably, the genetic variants resulted in loss of function with decreased expression or aberrant phosphorylation of the ERBB3/ERBB2 receptors. Experiments using mice revealed that Erbb3 and Erbb2 were expressed in enteric neuronal progenitor cells. This study is an outstanding example of descriptive observation that begs for mechanistic exploration to reveal precisely how the NRG1/ERBB3/ERBB2 pathway influences ENS development.
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