Evidence map›Paper›PMID 23376538›Full record

ReviewDevelopmental biology2013

Balancing on the crest - Evidence for disruption of the enteric ganglia via inappropriate lineage segregation and consequences for gastrointestinal function.

Melissa A Musser, E Michelle Southard-Smith

Abstract readReview
In one paragraph

Review in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Novel mutation-deletion in theJournal of genetic syndromes & gene therapy · 2015
    Article
  11. Enteric neuron imbalance and proximal dysmotility in ganglionated intestine of theCellular and molecular gastroenterology and hepatology · 2015
    Article
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.

Melissa A MusserDivision of Genetic Medicine, Department of Medicine and the PhD Program in Human Genetics, Center for Human Genetic Research, Vanderbilt University School of Medicine, Nashville, TN, USA.
E Michelle Southard-Smith

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Genetic Complexity and Modifiers of Hirschsprung DiseaseR01DK060047 · NIDDK · VANDERBILT UNIVERSITY · PI SOUTHARD-SMITH, E MICHELLE · 2002 to 2011
$3.6M
Enteric nervous system deficits in Hirschsprung ganglionic bowelF30DK096831 · NIDDK · VANDERBILT UNIVERSITY · PI MUSSER, MELISSA A · 2012 to 2014
$122k
NIDDK NIH HHS F30 DK096831NIDDK NIH HHS F30DK096831NIDDK NIH HHS R01 DK060047NIDDK NIH HHS R01DK60047NIGMS NIH HHS T32 GM007347
6 · The paper itself

Abstract

Normal enteric nervous system (ENS) development relies on numerous factors, including appropriate migration, proliferation, differentiation, and maturation of neural crest (NC) derivatives. Incomplete rostral to caudal migration of enteric neural crest-derived progenitors (ENPs) down the gut is at least partially responsible for the absence of enteric ganglia that is a hallmark feature of Hirschsprung disease (HSCR). The thought that ganglia proximal to aganglionosis are normal has guided surgical procedures for HSCR patients. However, chronic gastrointestinal dysfunction suffered by a subset of patients after surgery as well as studies in HSCR mouse models suggest that aberrant NC segregation and differentiation may be occurring in ganglionated regions of the intestine. Studies in mouse models that possess enteric ganglia throughout the length of the intestine (non-HSCR) have also found that certain genetic alterations affect neural crest lineage balance and interestingly many of these mutants also have functional gastrointestinal (GI) defects. It is possible that many GI disorders can be explained in part by imbalances in NC-derived lineages. Here we review studies evaluating ENS defects in HSCR and non-HSCR mouse models, concluding with clinical implications while highlighting areas requiring further study.

Indexed as

Cell LineageAnimalsEnteric Nervous SystemGangliaGastrointestinal TractHumansModels, BiologicalNeural CrestEnteric nervous systemGastrointestinal functionHirschsprung diseaseLineage segregationMouse modelsNeural crest development

Identifiers

PMID23376538
PMCPMC3672334

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Registered trials

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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.