Evidence map›Paper›PMID 29780380›Full record

ReviewFrontiers in immunology2018

Mitochondrial Damage-Associated Molecular Patterns: From Inflammatory Signaling to Human Diseases.

Serge Grazioli, Jérôme Pugin

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 250 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
250citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

250 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  20. TLR9-mediated innate immune signaling contributes to acetaminophen-induced injury in the developing lung.American journal of physiology. Lung cellular and molecular physiology · 2026
    Article

190 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

2 authors.

Serge GrazioliPediatric Intensive Care Unit, Department of Pediatrics, University Hospital of Geneva, University of Geneva, Geneva, Switzerland.
Jérôme PuginIntensive Care Unit, Department of Anesthesiology, Faculty of Medicine, University Hospital of Geneva, University of Geneva, Geneva, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the recent years, much has been unraveled about the pro-inflammatory properties of various mitochondrial molecules once they are leaving the mitochondrial compartment. On entering the cytoplasm or the extracellular space, mitochondrial DAMPs (also known as mitochondrial alarmins) can become pro-inflammatory and initiate innate and adaptive immune responses by activating cell surface and intracellular receptors. Current evidence indicates that uncontrolled and excessive release of mitochondrial DAMPs is associated with severity, has prognosis value in human diseases, and contributes to the dysregulated process observed in numerous inflammatory and autoimmune conditions, as well as in ischemic heart disease and cancer. Herein, we review that the expanding research field of mitochondrial DAMPs in innate immune responses and the current knowledge on the association between mitochondrial DAMPs and human diseases.

Indexed as

Immunity, InnateAlarminsAnimalsAutoimmune DiseasesCytokinesHumansInflammationMiceMitochondriaMyocardial IschemiaNeoplasmsSignal TransductionAlarminsCytokinesalarminsdamage-associated molecular patterninflammationmitochondriapro-inflammatory cytokinessterile inflammation

Identifiers

PMID29780380
PMCPMC5946030

What OpenQuestion holds

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Registered trials

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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.