Evidence map›Paper›PMID 30472725›Full record

ReviewClinical and experimental immunology2019

Behçet's syndrome as a tool to dissect the mechanisms of thrombo-inflammation: clinical and pathogenetic aspects.

M Becatti, G Emmi, A Bettiol, E Silvestri, G Di Scala, N Taddei, D Prisco, C Fiorillo

Open access · bronzeAbstract readReview
In one paragraph

Review in Clinical and experimental immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Trial
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  7. Review
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  9. Review
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  13. Review
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  15. Article
  16. Editorial: Molecular mechanisms of thrombosis.Frontiers in molecular biosciences · 2024
    Article
  17. Article
  18. Article
  19. Review
  20. SIRT1 and thrombosis.Frontiers in molecular biosciences · 2023
    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

8 authors at 1 institution in 1 country.

M BecattiDepartment of Experimental and Clinical Biomedical Sciences 'Mario Serio', University of Firenze, Italy.ORCID 0000-0002-2593-5908
G EmmiDepartment of Experimental and Clinical Medicine, University of Firenze, Italy.ORCID 0000-0001-9575-8321
A BettiolDepartment of Experimental and Clinical Medicine, University of Firenze, Italy.
E SilvestriDepartment of Experimental and Clinical Medicine, University of Firenze, Italy.
G Di ScalaDepartment of Experimental and Clinical Medicine, University of Firenze, Italy.
N TaddeiDepartment of Experimental and Clinical Biomedical Sciences 'Mario Serio', University of Firenze, Italy.
D PriscoDepartment of Experimental and Clinical Medicine, University of Firenze, Italy.
C FiorilloDepartment of Experimental and Clinical Biomedical Sciences 'Mario Serio', University of Firenze, Italy.
University of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Behçet's syndrome (BS) is a complex disease with different organ involvement. The vascular one is the most intriguing, considering the existence of a specific group of patients suffering from recurrent vascular events involving the venous and, more rarely, the arterial vessels. Several clinical clues suggest the inflammatory nature of thrombosis in BS, especially of the venous involvement, thus BS is considered a model of inflammation-induced thrombosis. Unique among other inflammatory conditions, venous involvement (together with the arterial one) is currently treated with immunosuppressants, rather than with anti-coagulants. Although many in-vitro studies have suggested the different roles of the multiple players involved in clot formation, in-vivo models are crucial to study this process in a physiological context. At present, no clear mechanisms describing the pathophysiology of thrombo-inflammation in BS exist. Recently, we focused our attention on BS patients as a human in-vivo model of inflammation-induced thrombosis to investigate a new mechanism of clot formation. Indeed, fibrinogen displays a critical role not only in inflammatory processes, but also in clot formation, both in the fibrin network and in platelet aggregation. Reactive oxygen species (ROS)-derived modifications represent the main post-translational fibrinogen alterations responsible for structural and functional changes. Recent data have revealed that neutrophils (pivotal in the pathogenetic mechanisms leading to BS damage) promote fibrinogen oxidation and thrombus formation in BS. Altogether, these new findings may help understand the pathogenetic bases of inflammation-induced thrombosis and, more importantly, may suggest potential targets for innovative therapeutic approaches.

Indexed as

Behcet SyndromeFibrinogenHumansImmunosuppressive AgentsInflammationReactive Oxygen SpeciesThrombosisFibrinogenImmunosuppressive AgentsReactive Oxygen SpeciesBehçet’s syndromefibrinogenneutrophilsoxidative stressthrombosis

Identifiers

PMID30472725
PMCPMC6378375
OpenAlexW2901537026

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.