Evidence map›Paper›PMID 37063765›Full record

ArticleResearch and practice in thrombosis and haemostasis2023

Novel mechanisms of thrombo-inflammation during infection: spotlight on neutrophil extracellular trap-mediated platelet activation.

Martina Colicchia, Gina Perrella, Poppy Gant, Julie Rayes

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Research and practice in thrombosis and haemostasis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06294730 (Coronary Microcirculation and Troponin Elevation in Septic Shock), which is not on this map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
7.4field-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.

NCT06294730 completednot on this map

Coronary Microcirculation and Troponin Elevation in Septic Shock

TypeobservationalSponsorKarolinska InstitutetRan2019 to 2025Enrolled62ConditionsSepsis, Myocardial Injury, Coronary Microvascular Dysfunction, Endothelial Dysfunction
3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Thromborepair: the tissue repair partner to thromboinflammation.Blood vessels, thrombosis & hemostasis · 2026
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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

4 authors at 2 institutions in 1 country.

Martina ColicchiaInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Vincent Drive, Birmingham, U.K.
Gina PerrellaInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Vincent Drive, Birmingham, U.K.
Poppy GantInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Vincent Drive, Birmingham, U.K.
Julie RayesInstitute of Cardiovascular Sciences, College of Medical and Dental Sciences, University of Birmingham, Vincent Drive, Birmingham, U.K.
University of Birmingham · GBWest Midlands Deanery · GB

Funding

British Heart Foundation FS/IBSRF/20/25039Wellcome Trust 204951
6 · The paper itself

Abstract

A state-of-the-art lecture titled "novel mechanisms of thrombo-inflammation during infection" was presented at the ISTH Congress in 2022. Platelet, neutrophil, and endothelial cell activation coordinate the development, progression, and resolution of thrombo-inflammatory events during infection. Activated platelets and neutrophil extracellular traps (NETs) are frequently observed in patients with sepsis and COVID-19, and high levels of NET-derived damage-associated molecular patterns (DAMPs) correlate with thrombotic complications. NET-associated DAMPs induce direct and indirect platelet activation, which in return potentiates neutrophil activation and NET formation. These coordinated interactions involve multiple receptors and signaling pathways contributing to vascular and organ damage exacerbating disease severity. This state-of-the-art review describes the main mechanisms by which platelets support NETosis and the key mechanisms by which NET-derived DAMPs trigger platelet activation and the formation of procoagulant platelets leading to thrombosis. We report how these DAMPs act through multiple receptors and signaling pathways differentially regulating cell activation and disease outcome, focusing on histones and S100A8/A9 and their contribution to the pathogenesis of sepsis and COVID-19. We further discuss the complexity of platelet activation during NETosis and the potential benefit of targeting selective or multiple NET-associated DAMPs to limit thrombo-inflammation during infection. Finally, we summarize relevant new data on this topic presented during the 2022 ISTH Congress.

Indexed as

DAMPshistonesNETosisplateletsS100A8/A9

Identifiers

PMID37063765
PMCPMC10099327
OpenAlexW4323923319

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.