Evidence map›Paper›PMID 37081895›Full record

ReviewFrontiers in immunology2023

Endothelial dysfunction and immunothrombosis in sepsis.

Eleni Maneta, Evmorfia Aivalioti, Simon Tual-Chalot, Besa Emini Veseli, Aikaterini Gatsiou, Kimon Stamatelopoulos, Konstantinos Stellos

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed, 4 pooled it
22.2field-weighted citation impact, top 1% 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

132 citing papers in PubMed, 4 syntheses or guidelines pooled it, 135 citations in OpenAlex.

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72 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

7 authors at 4 institutions in 3 countries.

Eleni ManetaDepartment of Clinical Therapeutics, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Evmorfia AivaliotiDepartment of Clinical Therapeutics, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Simon Tual-ChalotBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Besa Emini VeseliDepartment of Cardiovascular Research, European Center for Angioscience (ECAS), Heidelberg University, Mannheim, Germany.
Aikaterini GatsiouBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Kimon StamatelopoulosDepartment of Clinical Therapeutics, National and Kapodistrian University of Athens Medical School, Athens, Greece.
Konstantinos StellosBiosciences Institute, Vascular Biology and Medicine Theme, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne, United Kingdom.
Newcastle University · GBNational and Kapodistrian University of Athens · GRGerman Centre for Cardiovascular Research · DEHeidelberg University · DE

Funding

Biotechnology and Biological Sciences Research CouncilWellcome Trust
6 · The paper itself

Abstract

Sepsis is a life-threatening clinical syndrome characterized by multiorgan dysfunction caused by a dysregulated or over-reactive host response to infection. During sepsis, the coagulation cascade is triggered by activated cells of the innate immune system, such as neutrophils and monocytes, resulting in clot formation mainly in the microcirculation, a process known as immunothrombosis. Although this process aims to protect the host through inhibition of the pathogen's dissemination and survival, endothelial dysfunction and microthrombotic complications can rapidly lead to multiple organ dysfunction. The development of treatments targeting endothelial innate immune responses and immunothrombosis could be of great significance for reducing morbidity and mortality in patients with sepsis. Medications modifying cell-specific immune responses or inhibiting platelet-endothelial interaction or platelet activation have been proposed. Herein, we discuss the underlying mechanisms of organ-specific endothelial dysfunction and immunothrombosis in sepsis and its complications, while highlighting the recent advances in the development of new therapeutic approaches aiming at improving the short- or long-term prognosis in sepsis.

Indexed as

SepsisThrombosisVascular DiseasesHumansNeutrophilsThromboinflammationendothelial dysfunctionimmunothrombosisneutrophil extracellular trapssepsistissue factor

Identifiers

PMID37081895
PMCPMC10110956
OpenAlexW4362561278

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.