Evidence map›Paper›PMID 31629396›Full record

ReviewCurrent neuropharmacology2020

The Contribution of Formyl Peptide Receptor Dysfunction to the Course of Neuroinflammation: A Potential Role in the Brain Pathology.

Ewa Trojan, Natalia Bryniarska, Monika Leśkiewicz, Magdalena Regulska, Katarzyna Chamera, Magdalena Szuster-Głuszczak, Marcello Leopoldo, Enza Lacivita, Agnieszka Basta-Kaim

Open access · greenAbstract readReview
In one paragraph

Review in Current neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 36 citations in OpenAlex.

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  14. Annexin A1 in the nervous and ocular systems.Neural regeneration research · 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

9 authors at 3 institutions in 2 countries.

Ewa TrojanLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Natalia BryniarskaLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Monika LeśkiewiczLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Magdalena RegulskaLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Katarzyna ChameraLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Magdalena Szuster-GłuszczakLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Marcello LeopoldoDepartment of Pharmacy - Drug Sciences, University of Bari, via Orabona 4, 70125 Bari, Italy.
Enza LacivitaDepartment of Pharmacy - Drug Sciences, University of Bari, via Orabona 4, 70125 Bari, Italy.
Agnieszka Basta-KaimLaboratory of Immunoendocrinology, Department of Experimental Neuroendocrinology, Maj Institute of Pharmacology, Polish Academy of Sciences, 12 Smetna St. 31-343 Krakow, Poland.
Maj Institute of Pharmacology · PLPolish Academy of Sciences · PLUniversity of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic inflammatory processes within the central nervous system (CNS) are in part responsible for the development of neurodegenerative and psychiatric diseases. These processes are associated with, among other things, the increased and disturbed activation of microglia and the elevated production of proinflammatory factors. Recent studies indicated that the disruption of the process of resolution of inflammation (RoI) may be the cause of CNS disorders. It is shown that the RoI is regulated by endogenous molecules called specialized pro-resolving mediators (SPMs), which interact with specific membrane receptors. Some SPMs activate formyl peptide receptors (FPRs), which belong to the family of seven-transmembrane G protein-coupled receptors. These receptors take part not only in the proinflammatory response but also in the resolution of the inflammation process. Therefore, the activation of FPRs might have complex consequences. This review discusses the potential role of FPRs, and in particular the role of FPR2 subtype, in the brain under physiological and pathological conditions and their involvement in processes underlying neurodegenerative and psychiatric disorders as well as ischemia, the pathogenesis of which involves the dysfunction of inflammatory processes.

Indexed as

AnimalsAstrocytesBrainBrain IschemiaEncephalitisHumansMicrogliaReceptors, Formyl PeptideReceptors, Formyl PeptideAlzheimer's diseasedepressionformyl peptide receptorsglial cellsischemiaNeuroinflammationnew pro-resolving agonistsresolution of inflammation.

Identifiers

PMID31629396
PMCPMC7327951
OpenAlexW2980873684

What Socratic holds

Textmetadata
LicenceCC BY-NC
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 Socratic graph.