Evidence map›Paper›PMID 28492466›Full record

ReviewInternational journal of molecular sciences2017

NGF and Its Receptors in the Regulation of Inflammatory Response.

Gaetana Minnone, Fabrizio De Benedetti, Luisa Bracci-Laudiero

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 185 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 2 pooled it
9.2field-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

185 citing papers in PubMed, 2 syntheses or guidelines pooled it, 317 citations in OpenAlex.

  1. Clinics in orthopedic surgery · 2025
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125 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

3 authors at 2 institutions in 1 country.

Gaetana MinnoneDivision of Rheumatology and Immuno-Rheumatology Research Laboratories, Bambino Gesù Children's Hospital, 00146 Rome, Italy. gaetana.minnone@yahoo.it.
Fabrizio De BenedettiDivision of Rheumatology and Immuno-Rheumatology Research Laboratories, Bambino Gesù Children's Hospital, 00146 Rome, Italy. fabrizio.debenedetti@opbg.net.
Luisa Bracci-LaudieroDivision of Rheumatology and Immuno-Rheumatology Research Laboratories, Bambino Gesù Children's Hospital, 00146 Rome, Italy. luisa.braccilaudiero@ift.cnr.it.
Bambino Gesù Children's Hospital · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

There is growing interest in the complex relationship between the nervous and immune systems and how its alteration can affect homeostasis and result in the development of inflammatory diseases. A key mediator in cross-talk between the two systems is nerve growth factor (NGF), which can influence both neuronal cell function and immune cell activity. The up-regulation of NGF described in inflamed tissues of many diseases can regulate innervation and neuronal activity of peripheral neurons, inducing the release of immune-active neuropeptides and neurotransmitters, but can also directly influence innate and adaptive immune responses. Expression of the NGF receptors tropomyosin receptor kinase A (TrkA) and p75 neurotrophin receptor (p75NTR) is dynamically regulated in immune cells, suggesting a varying requirement for NGF depending on their state of differentiation and functional activity. NGF has a variety of effects that can be either pro-inflammatory or anti-inflammatory. This apparent contradiction can be explained by considering NGF as part of an endogenous mechanism that, while activating immune responses, also activates pathways necessary to dampen the inflammatory response and limit tissue damage. Decreases in TrkA expression, such as that recently demonstrated in immune cells of arthritis patients, might prevent the activation by NGF of regulatory feed-back mechanisms, thus contributing to the development and maintenance of chronic inflammation.

Indexed as

Adaptive ImmunityAnimalsArthritisCell DifferentiationCytokinesHumansImmunity, InnateInflammationMiceNerve Growth FactorNerve Tissue ProteinsNeuronsNeuropeptidesRatsReceptors, Nerve Growth FactorReceptor, trkACytokinesNerve Growth FactorNerve Tissue ProteinsNeuropeptidesNGFR protein, humanNTRK1 protein, humanReceptors, Nerve Growth FactorReceptor, trkAinflammatory diseasesinnate immunityneuropeptidesneurotransmitterssensory sympathetic and parasympathetic neurons

Identifiers

PMID28492466
PMCPMC5454940
OpenAlexW2612221856

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.