Evidence map›Paper›PMID 31019207›Full record

ArticleScientific reports2019

Amyloid β-dependent mitochondrial toxicity in mouse microglia requires P2X7 receptor expression and is prevented by nimodipine.

Paola Chiozzi, Alba Clara Sarti, Juana M Sanz, Anna Lisa Giuliani, Elena Adinolfi, Valentina Vultaggio-Poma, Simonetta Falzoni, Francesco Di Virgilio

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.

  1. Pooled it
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  6. Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026
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  11. Calcium Ions in the Physiology and Pathology of the Central Nervous System.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. 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

8 authors at 1 institution in 1 country.

Paola ChiozziDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Alba Clara SartiDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Juana M SanzDepartment of Medical Sciences, University of Ferrara, Ferrara, Italy.
Anna Lisa GiulianiDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Elena AdinolfiDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Valentina Vultaggio-PomaDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Simonetta FalzoniDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy.
Francesco Di VirgilioDepartment of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy. fdv@unife.it.ORCID http://orcid.org/0000-0003-3566-1362
University of Ferrara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous data from our laboratory show that expression of the P2X7 receptor (P2X7R) is needed for amyloid β (Aβ)-stimulated microglia activation and IL-1β release in vitro and in vivo. We also showed that Aβ-dependent stimulation is inhibited by the dihydropyridine nimodipine at an intracellular site distal to the P2X7R. In the present study, we used the N13 microglia cell line and mouse primary microglia from wt and P2rx7-deleted mice to test the effect of nimodipine on amyloid β (Aβ)-dependent NLRP3 inflammasome expression and function, and on mitochondrial energy metabolism. Our data show that in microglia Aβ causes P2X7R-dependent a) NFκB activation; b) NLRP3 inflammasome expression and function; c) mitochondria toxicity; and these changes are fully inhibited by nimodipine. Our study shows that nimodipine is a powerful blocker of cell damage caused by monomeric and oligomeric Aβ, points to the mitochondria as a crucial target, and underlines the permissive role of the P2X7R.

Indexed as

Amyloid beta-PeptidesAnimalsCalcium Channel BlockersCell LineCells, CulturedFemaleInflammasomesInterleukin-1betaMaleMice, Inbred C57BLMice, KnockoutMicrogliaMitochondriaNimodipineNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, Purinergic P2X7Amyloid beta-PeptidesCalcium Channel BlockersInflammasomesInterleukin-1betaNimodipineNLR Family, Pyrin Domain-Containing 3 ProteinReceptors, Purinergic P2X7

Identifiers

PMID31019207
PMCPMC6482182
OpenAlexW2942190095

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.