Evidence map›Paper›PMID 27918427›Full record

ReviewInternational journal of molecular sciences2016

Prolactin: Friend or Foe in Central Nervous System Autoimmune Inflammation?

Massimo Costanza, Rosetta Pedotti

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

  1. Opioid Signaling in Multiple Sclerosis: Emerging Targets for Repair.International journal of molecular sciences · 2026
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  12. The role of prolactin/vasoinhibins in cardiovascular diseases.Animal models and experimental medicine · 2023
    Review
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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.

Massimo CostanzaDepartment of Clinical Neuroscience, Neurological Institute Foundation IRCCS Carlo Besta, 20133 Milan, Italy. Massimo.Costanza@istituto-besta.it.
Rosetta PedottiDepartment of Clinical Neuroscience, Neurological Institute Foundation IRCCS Carlo Besta, 20133 Milan, Italy. Rosetta.Pedotti@istituto-besta.it.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The higher prevalence of multiple sclerosis (MS) in females, along with the modulation of disease activity observed during pregnancy and the post-partum period, has suggested a hormonal influence in MS. Even if prolactin (PRL) does not belong to the sex hormones family, its crucial role in female reproduction and lactation has prompted great efforts to understand if PRL could represent a gender factor in the pathogenesis of MS and experimental autoimmune encephalomyelitis (EAE), the animal model for this disease. Extensive literature has documented a remarkable immune-stimulating potential for this hormone, indicating PRL as a disease-promoting factor in MS and EAE. However, recent work has pointed out that PRL is endowed with important neuroprotective and remyelinating properties and has encouraged a reinterpretation of the involvement of this hormone in MS. In this review we summarize both the protective functions that PRL exerts in central nervous system tissue as well as the inflammatory activity of this hormone in the context of autoimmune responses against myelin. Last, we draw future lines of research that might help to better clarify the impact of PRL on MS pathology.

Indexed as

AnimalsCentral Nervous SystemEncephalomyelitis, Autoimmune, ExperimentalHumansModels, BiologicalProlactinProlactinexperimental autoimmune encephalomyelitismultiple sclerosisneuroinflammationneuroprotectionprolactin

Identifiers

PMID27918427
PMCPMC5187826
OpenAlexW2559520268

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.