Evidence map›Paper›PMID 38815564›Full record

ReviewJournal of innate immunity2024

Unraveling the Intricate Web: Complement Activation Shapes the Pathogenesis of Sepsis-Induced Coagulopathy.

Xin Wei, Ye Tu, Shuhong Bu, Guimei Guo, Hongbin Wang, Zhibin Wang

Abstract readReview
In one paragraph

Review in Journal of innate immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–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

17 citing papers in PubMed.

  1. Article
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  9. Disseminated intravascular coagulation.Journal of intensive care · 2025
    Review
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  11. Article
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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

6 authors.

Xin WeiDepartment of Clinical Pharmacy, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Ye TuDepartment of Pharmacy, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Shuhong BuDepartment of Clinical Pharmacy, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Guimei GuoDepartment of Pediatric Nephrology and Rheumatology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Hongbin WangMaster Program of Pharmaceutical Scieneces College of Graduate Studies, Department of Pharmaceutical and Biomedical Sciences College of Pharmacy, Department of Basic Science College of Medicine, California Northstate University, Elk Grove, California, USA.
Zhibin WangDepartment of Critical Care Medicine, School of Anesthesiology, Naval Medical University, Shanghai, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSepsis-associated coagulopathy specifically refers to widespread systemic coagulation activation accompanied by a high risk of hemorrhage and organ damage, which in severe cases manifests as disseminated intravascular coagulation (DIC), or even develops into multiple organ dysfunction syndrome (MODS). The complement system and the coagulation system as the main columns of innate immunity and hemostasis, respectively, undergo substantial activation after sepsis. SUMMARY: Dysfunction of the complement, coagulation/fibrinolytic cascades caused by sepsis leads to "thromboinflammation," which ultimately amplifies the systemic inflammatory response and accelerates the development of MODS. Recent studies have revealed that massive activation of the complement system exacerbates sepsis-induced coagulation and even results in DIC, which suggests that inhibition of complement activation may have therapeutic potential in the treatment of septic coagulopathy. KEY MESSAGES: Sepsis-associated thrombosis involves the upregulation or activation of procoagulant factors, down-regulation or inactivation of anticoagulant factors, and impairment of the fibrinolytic mechanism. This review aims to summarize the latest literature and analyze the underlying molecular mechanisms of the activation of the complement system on the abnormal coagulation cascades in sepsis.

Indexed as

Complement ActivationSepsisAnimalsBlood CoagulationBlood Coagulation DisordersComplement System ProteinsDisseminated Intravascular CoagulationFibrinolysisHumansImmunity, InnateMultiple Organ FailureThrombosisComplement System ProteinsComplementSepsis-associated coagulopathyThromboinflammation

Identifiers

PMID38815564
PMCPMC11249610

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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.