Evidence map›Paper›PMID 30923524›Full record

ReviewFrontiers in immunology2019

Complement in the Pathophysiology of the Antiphospholipid Syndrome.

Shruti Chaturvedi, Robert A Brodsky, Keith R McCrae

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 2 pooled it
13.4field-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

72 citing papers in PubMed, 2 syntheses or guidelines pooled it, 130 citations in OpenAlex.

  1. Pooled it
  2. Pediatric APS: State of the Art.Current rheumatology reports · 2020
    Pooled it
  3. Observational
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. C4b-binding protein as an antigenic target in the pathogenesis of antiphosphatidylethanolamine autoantibodies.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  10. Review
  11. Article
  12. Animal models of antiphospholipid syndrome.Frontiers in immunology · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Complement System Inhibitors in Nephrology: An Update-Narrative Review.International journal of molecular sciences · 2025
    Review

12 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

3 authors at 3 institutions in 1 country.

Shruti ChaturvediDivision of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Robert A BrodskyDivision of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, United States.
Keith R McCraeHematologic Oncology and Blood Disorders, Taussig Cancer Institute, Cleveland, OH, United States.
Cleveland Clinic · USJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

Complementopathies: Genotype and PhenotypeR01HL133113 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BRODSKY, ROBERT A · 2016 to 2020
$2.0M
Transcriptional control of endothelium in APS by Kruppel Like factorsR01HL123098 · NHLBI · CLEVELAND CLINIC LERNER COM-CWRU · PI JAIN, MUKESH KUMAR, MCCRAE, KEITH R. · 2014 to 2017
$1.8M
NHLBI NIH HHS R01 HL123098NHLBI NIH HHS R01 HL133113
6 · The paper itself

Abstract

The antiphospholipid syndrome (APS) is characterized by thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). Complement is a system of enzymes and regulatory proteins of the innate immune system that plays a key role in the inflammatory response to pathogenic stimuli. The complement and coagulation pathways are closely linked, and expanding data indicate that complement may be activated in patients with aPL and function as a cofactor in the pathogenesis of aPL-associated clinical events. Complement activation by aPL generates C5a, which induces neutrophil tissue factor-dependent procoagulant activity. Beta-2-glycoprotein I, the primary antigen for pathogenic aPL, has complement regulatory effects

Indexed as

Antiphospholipid SyndromeComplement ActivationPregnancy ComplicationsThrombotic MicroangiopathiesAnimalsAntibodies, AntiphospholipidAntibodies, Monoclonal, HumanizedComplement System ProteinsFemaleHumansMicePregnancyAntibodies, AntiphospholipidAntibodies, Monoclonal, HumanizedComplement System Proteinseculizumabantiphosholipid antibodiesbeta2 - glycoprotein Icomplementendothelialthrombosis

Identifiers

PMID30923524
PMCPMC6426753
OpenAlexW2920903673

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.