Evidence map›Paper›PMID 33276665›Full record

ReviewInternational journal of molecular sciences2020

Enteric Glia at the Crossroads between Intestinal Immune System and Epithelial Barrier: Implications for Parkinson Disease.

Laura Benvenuti, Vanessa D'Antongiovanni, Carolina Pellegrini, Luca Antonioli, Nunzia Bernardini, Corrado Blandizzi, Matteo Fornai

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 2 pooled it
3.2field-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

33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 51 citations in OpenAlex.

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  13. Gastrointestinal dysmotility in rodent models of Parkinson's disease.American journal of physiology. Gastrointestinal and liver physiology · 2024
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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

7 authors at 1 institution in 1 country.

Laura BenvenutiDepartment of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
Vanessa D'AntongiovanniDepartment of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
Carolina PellegriniDepartment of Pharmacy, University of Pisa, 56126 Pisa, Italy.
Luca AntonioliDepartment of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
Nunzia BernardiniDepartment of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
Corrado BlandizziDepartment of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
Matteo FornaiDepartment of Clinical and Experimental Medicine, University of Pisa, 56126 Pisa, Italy.
University of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over recent years, several investigations have suggested that Parkinson's disease (PD) can be regarded as the consequence of a bowel disorder. Indeed, gastrointestinal symptoms can occur at all stages of this neurodegenerative disease and in up to a third of cases, their onset can precede the involvement of the central nervous system. Recent data suggest that enteric glial cells (EGCs) may play a major role in PD-related gastrointestinal disturbances, as well as in the development and progression of the central disease. In addition to their trophic and structural functions, EGCs are crucial for the homeostatic control of a wide range of gastrointestinal activities. The main purpose of this review was to provide a detailed overview of the role of EGCs in intestinal PD-associated alterations, with particular regard for their participation in digestive and central inflammation as well as the dynamic interactions between glial cells and intestinal epithelial barrier. Accumulating evidence suggests that several pathological intestinal conditions, associated with an impairment of barrier permeability, may trigger dysfunctions of EGCs and their shift towards a proinflammatory phenotype. The reactive gliosis is likely responsible for PD-related neuroinflammation and the associated pathological changes in the ENS. Thus, ameliorating the efficiency of mucosal barrier, as well as avoiding IEB disruption and the related reactive gliosis, might theoretically prevent the onset of PD or, at least, counteract its progression.

Indexed as

Signal Transductionalpha-SynucleinAnimalsBrainEnteric Nervous SystemGastrointestinal MicrobiomeHumansIntestinal MucosaNeurogliaParkinson Diseasealpha-Synucleinenteric glial cellsenteric immune systemgut–brain axisintestinal epithelial barrierParkinson’s diseaseα-synuclein

Identifiers

PMID33276665
PMCPMC7730281
OpenAlexW3108336334

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.