Evidence map›Paper›PMID 26899371›Full record

ArticleScientific reports2016

High-throughput proteomics reveal alarmins as amplifiers of tissue pathology and inflammation after spinal cord injury.

Athanasios Didangelos, Michele Puglia, Michaela Iberl, Candela Sanchez-Bellot, Bernd Roschitzki, Elizabeth J Bradbury

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  4. Extracellular matrix remodeling supportsbioRxiv : the preprint server for biology · 2025
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  7. Article
  8. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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3 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

6 authors at 2 institutions in 2 countries.

Athanasios DidangelosWolfson Center for Age Related Diseases, Guys Campus, King's College London, United Kingdom.
Michele PugliaFunctional Genomics Center Zurich (FGCZ), ETH Zurich, University of Zurich, Switzerland.
Michaela IberlWolfson Center for Age Related Diseases, Guys Campus, King's College London, United Kingdom.
Candela Sanchez-BellotWolfson Center for Age Related Diseases, Guys Campus, King's College London, United Kingdom.
Bernd RoschitzkiFunctional Genomics Center Zurich (FGCZ), ETH Zurich, University of Zurich, Switzerland.
Elizabeth J BradburyWolfson Center for Age Related Diseases, Guys Campus, King's College London, United Kingdom.
King's College London · GBETH Zurich · CH

Funding

Medical Research Council G1002055
6 · The paper itself

Abstract

Spinal cord injury is characterized by acute cellular and axonal damage followed by aggressive inflammation and pathological tissue remodelling. The biological mediators underlying these processes are still largely unknown. Here we apply an innovative proteomics approach targeting the enriched extracellular proteome after spinal cord injury for the first time. Proteomics revealed multiple matrix proteins not previously associated with injured spinal tissue, including small proteoglycans involved in cell-matrix adhesion and collagen fibrillogenesis. Network analysis of transcriptomics and proteomics datasets uncovered persistent overexpression of extracellular alarmins that can trigger inflammation via pattern recognition receptors. In mechanistic experiments, inhibition of toll-like receptor-4 (TLR4) and the receptor for advanced glycation end-products (RAGE) revealed the involvement of alarmins in inflammatory gene expression, which was found to be dominated by IL1 and NFκΒ signalling. Extracellular high-mobility group box-1 (HMGB1) was identified as the likely endogenous regulator of IL1 expression after injury. These data reveal a novel tissue remodelling signature and identify endogenous alarmins as amplifiers of the inflammatory response that promotes tissue pathology and impedes neuronal repair after spinal cord injury.

Indexed as

AlarminsAnimalsCell-Matrix JunctionsGene Expression RegulationHigh-Throughput Screening AssaysHMGB1 ProteinHumansInflammationInterleukin-1NeuronsProteomicsRatsReceptor for Advanced Glycation End ProductsSignal TransductionSpinal Cord InjuriesToll-Like Receptor 4Ager protein, ratAlarminsHMGB1 ProteinInterleukin-1Receptor for Advanced Glycation End ProductsTlr4 protein, ratToll-Like Receptor 4

Identifiers

PMID26899371
PMCPMC4761922
OpenAlexW2284184435

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.