Evidence map›Paper›PMID 31604034›Full record

ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2019

Enteric neuroplasticity and dysmotility in inflammatory disease: key players and possible therapeutic targets.

Estelle T Spear, Gary M Mawe

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Gastrointestinal and liver physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. Enteric nervous system as a therapeutic target in gastrointestinal disorders.World journal of gastrointestinal pharmacology and therapeutics · 2025
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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 2 institutions in 1 country.

Estelle T SpearDivision of Gastroenterology and Hepatology, Department of Medicine, School of Medicine, Stanford University, Stanford, California.
Gary M MaweDepartment of Neurological Sciences, The University of Vermont, Burlington, Vermont.
Stanford University · USUniversity of Vermont · US

Funding

Autoimmune mechanisms of gastrointestinal dysmotility in multiple sclerosisR01DK113800 · NIDDK · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI MAWE, GARY M · 2017 to 2020
$1.8M
Intestinal Dysmotility in Multiple SclerosisF31DK108540 · NIDDK · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BISHOP, ESTELLE SPEAR · 2016 to 2017
$55k
NIDDK NIH HHS F31 DK108540NIDDK NIH HHS R01 DK113800
6 · The paper itself

Abstract

Intestinal functions, including motility and secretion, are locally controlled by enteric neural networks housed within the wall of the gut. The fidelity of these functions depends on the precision of intercellular signaling among cellular elements, including enteric neurons, epithelial cells, immune cells, and glia, all of which are vulnerable to disruptive influences during inflammatory events. This review article describes current knowledge regarding inflammation-induced neuroplasticity along key elements of enteric neural circuits, what is known about the causes of these changes, and possible therapeutic targets for protecting and/or repairing the integrity of intrinsic enteric neurotransmission. Changes that have been detected in response to inflammation include increased epithelial serotonin availability, hyperexcitability of intrinsic primary afferent neurons, facilitation of synaptic activity among enteric neurons, and attenuated purinergic neuromuscular transmission. Dysfunctional propulsive motility has been detected in models of colitis, where causes include the changes described above, and in models of multiple sclerosis and other autoimmune conditions, where autoantibodies are thought to mediate dysmotility. Other cells implicated in inflammation-induced neuroplasticity include muscularis macrophages and enteric glia. Targeted treatments that are discussed include

Indexed as

Enteric Nervous SystemInflammationAnimalsCell CommunicationGastrointestinal MotilityHumansNervous System Autoimmune Disease, ExperimentalNeuronal Plasticityautoantibodyenteric nervous systemgastrointestinal motilitygliamacrophage

Identifiers

PMID31604034
PMCPMC6962496
OpenAlexW2979626005

What OpenQuestion holds

Textmetadata
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.