Evidence map›Paper›PMID 32915348›Full record

ArticleJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2020

Mitochondria Regulate Inflammatory Paracrine Signalling in Neurodegeneration.

Danilo Faccenda, Michelangelo Campanella

Abstract readLetter
PubMed Publisher
In one paragraph

Article in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 51% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
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 at 1 institution in 1 country.

Danilo FaccendaDepartment of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, Royal College Street, London, NW1 0TU, UK.
Michelangelo CampanellaDepartment of Comparative Biomedical Sciences, The Royal Veterinary College, University of London, Royal College Street, London, NW1 0TU, UK. mcampanella@rvc.ac.uk.
Royal Veterinary College · GB

Funding

Biotechnology and Biological Sciences Research Council BB/M010384/1Biotechnology and Biological Sciences Research Council BB/N007042/1
6 · The paper itself

Abstract

Mitochondrial dysfunction occurs in most neurodegenerative diseases, contributing to both their onset and progression. A recent breakthrough unveiled that propagation of the inflammatory response and subsequent neuronal injury are also mediated extracellularly by damaged mitochondria, which are released from active microglial cells into the brain milieu. These extracellular fragmented mitochondria can therefore generate sufficient toxicity to trigger neuronal death and widespread brain damage through activation of naïve astrocytes. Besides suggesting potential new pharmacological strategies of therapeutic intervention in neurodegeneration, this original work indicates that mitochondria might act as bioactive ligands exerting paracrine functions. This is an interesting, novel and impactful concept that deserves consideration by the scientific community, as the attention should now be focused on the identification of the specific receptors through which mitochondria mediate such an important extracellular signalling mechanism in neurological conditions.

Indexed as

HumansInflammation MediatorsMitochondriaNeurodegenerative DiseasesParacrine CommunicationSignal TransductionInflammation MediatorsExtracellular signallingMitochondriaNeurodegeneration

Identifiers

PMID32915348
OpenAlexW3086445465

What OpenQuestion holds

Textmetadata
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.