Evidence map›Paper›PMID 23639815›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2013

Enteric nervous system development: migration, differentiation, and disease.

Jonathan I Lake, Robert O Heuckeroth

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers.

0numbers the graph read from it
0cells of the map it votes in
206citing papers in PubMed
27.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

206 citing papers in PubMed, 380 citations in OpenAlex.

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  16. Endothelin-3 and T-type CaNature communications · 2026
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146 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jonathan I LakeDepartment of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.
Robert O Heuckeroth
Washington University in St. Louis · US

Funding

VITAMIN A DEFICIENCY AND INTESTINAL MOTILITY DISORDERSR01DK087715 · NIDDK · WASHINGTON UNIVERSITY · PI HEUCKEROTH, ROBERT O · 2010 to 2013
$1.3M
NIDDK NIH HHS R01 DK-087715NIDDK NIH HHS R01 DK087715
6 · The paper itself

Abstract

The enteric nervous system (ENS) provides the intrinsic innervation of the bowel and is the most neurochemically diverse branch of the peripheral nervous system, consisting of two layers of ganglia and fibers encircling the gastrointestinal tract. The ENS is vital for life and is capable of autonomous regulation of motility and secretion. Developmental studies in model organisms and genetic studies of the most common congenital disease of the ENS, Hirschsprung disease, have provided a detailed understanding of ENS development. The ENS originates in the neural crest, mostly from the vagal levels of the neuraxis, which invades, proliferates, and migrates within the intestinal wall until the entire bowel is colonized with enteric neural crest-derived cells (ENCDCs). After initial migration, the ENS develops further by responding to guidance factors and morphogens that pattern the bowel concentrically, differentiating into glia and neuronal subtypes and wiring together to form a functional nervous system. Molecules controlling this process, including glial cell line-derived neurotrophic factor and its receptor RET, endothelin (ET)-3 and its receptor endothelin receptor type B, and transcription factors such as SOX10 and PHOX2B, are required for ENS development in humans. Important areas of active investigation include mechanisms that guide ENCDC migration, the role and signals downstream of endothelin receptor type B, and control of differentiation, neurochemical coding, and axonal targeting. Recent work also focuses on disease treatment by exploring the natural role of ENS stem cells and investigating potential therapeutic uses. Disease prevention may also be possible by modifying the fetal microenvironment to reduce the penetrance of Hirschsprung disease-causing mutations.

Indexed as

AnimalsBody PatterningEnteric Nervous SystemGastrointestinal TractGene Expression Regulation, DevelopmentalHirschsprung DiseaseHumansNeural Crestaxonal targetingcell migrationchain migrationdevelopmententeric nervous systemgene-environment interactionsgenetic interactionsHirschsprung diseaseneural crestneural crest-derived stem cellsneurochemical codingpseudoobstruction

Identifiers

PMID23639815
PMCPMC3725693
OpenAlexW2095591360

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.