Evidence map›Paper›PMID 28129662›Full record

ReviewSeminars in thrombosis and hemostasis2018

New Insights in the Pathophysiology of Antiphospholipid Syndrome.

Anastasia Sacharidou, Philip W Shaul, Chieko Mineo

Abstract readReview
In one paragraph

Review in Seminars in thrombosis and hemostasis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  7. The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023
    Review
  8. Article
  9. Triple Positive Antiphospholipid Antibody Syndrome in Pregnancy with High Frequency Plasma Exchange: A Case Report.Transfusion medicine and hemotherapy : offizielles Organ der Deutschen Gesellschaft fur Transfusionsmedizin und Immunhamatologie · 2023
    Article
  10. An Overview of Laboratory Testing for Antiphospholipid Antibodies.Methods in molecular biology (Clifton, N.J.) · 2023
    Review
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  15. 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

3 authors at 1 institution in 1 country.

Anastasia SacharidouDepartment of Pediatrics, Center for Pulmonary and Vascular Biology, University of Texas Southwestern Medical Center, Dallas, Texas.
Philip W ShaulDepartment of Pediatrics, Center for Pulmonary and Vascular Biology, University of Texas Southwestern Medical Center, Dallas, Texas.
Chieko MineoDepartment of Pediatrics, Center for Pulmonary and Vascular Biology, University of Texas Southwestern Medical Center, Dallas, Texas.
The University of Texas Southwestern Medical Center · US

Funding

TRAINING PROGRAM IN LUNG BIOLOGY AND DISEASET32HL098040 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI SHAUL, PHILIP W, TERADA, LANCE S · 2009 to 2024
$4.6M
Role of Endothelial and Macrophage ApoER2 in Atherosclerosis ModulationR01HL118001 · NHLBI · UNIVERSITY OF CINCINNATI · PI HUI, DAVID YIU-KWAN, SHAUL, PHILIP W · 2014 to 2017
$2.8M
(PQ1) Epigenetic effects of the premalignant fieldR01CA208620 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TERADA, LANCE S · 2016 to 2020
$1.9M
Molecular Basis of Pregnancy Complications in the Antiphospholipid SyndromeR01HD094395 · NICHD · UT SOUTHWESTERN MEDICAL CENTER · PI MINEO, CHIEKO · 2018 to 2022
$1.8M
Endothelial Basis of Obesity-induced Insulin ResistanceR01DK110127 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI MINEO, CHIEKO · 2016 to 2019
$1.8M
Discovery of Novel Interventions of the Antiphospholipid SyndromeR01HL109604 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI MINEO, CHIEKO · 2011 to 2014
$1.6M
NCI NIH HHS R01 CA208620NHLBI NIH HHS R01 HL109604NHLBI NIH HHS R01 HL118001NHLBI NIH HHS T32 HL098040NICHD NIH HHS R01 HD094395NIDDK NIH HHS R01 DK110127
6 · The paper itself

Abstract

The antiphospholipid syndrome (APS) is an autoimmune disorder characterized by an elevated risk for arterial and venous thrombosis and pregnancy-related morbidity. Since the discovery of the disease in 1980s, numerous studies in cell culture systems, in animal models, and in patient populations have been reported, leading to a deeper understanding of the pathogenesis of APS. These studies have determined that circulating autoantibodies, collectively called antiphospholipid antibodies (aPL), the majority of which recognize cell surface proteins attached to the plasma membrane phospholipids, play a causal role in the development of the disease. The binding of aPL to the cell surface antigens triggers interaction of the complex with transmembrane receptors to initiate intracellular signaling in critical cell types, including platelets, monocytes, endothelial cells, and trophoblasts. Subsequent alteration of various cell functions results in inflammation, thrombus formation, and pregnancy complications. Apolipoprotein E receptor 2 (apoER2), a lipoprotein receptor family member, has been implicated as a mediator for aPL actions in platelets and endothelial cells. Nitric oxide (NO) is a signaling molecule known to exert potent antithrombotic, anti-inflammatory, and anti-atherogenic effects. NO insufficiency and oxidative stress have been linked to APS pathogenesis. This review will focus on the recent findings on how apoER2 and dysregulation of NO production contribute to aPL-mediated pathologies in APS.

Indexed as

Antiphospholipid SyndromeFemaleHumans

Identifiers

PMID28129662
PMCPMC6333209
OpenAlexW2581710795

What OpenQuestion holds

Textmetadata
LicenceTDM
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.