Evidence map›Paper›PMID 32702157›Full record

ReviewJournal of thrombosis and haemostasis : JTH2020

Vascular thiol isomerases in thrombosis: The yin and yang.

Yi Wu, David W Essex

Open access · greenAbstract readReview
In one paragraph

Review in Journal of thrombosis and haemostasis : JTH, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.3field-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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Estimate of Numbers of Disulfide-Bonded Protein States.Methods in molecular biology (Clifton, N.J.) · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Thiol isomerase ERp18 enhances platelet activation and arterial thrombosis.Research and practice in thrombosis and haemostasis · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. ERp57/PDIA3: new insight.Cellular & molecular biology letters · 2022
    Review
  20. Selective Secretion of KDEL-Bearing Proteins: Mechanisms and Functions.Frontiers in cell and developmental biology · 2022
    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

2 authors at 1 institution in 1 country.

Yi WuSol Sherry Thrombosis Center, Department of Medicine/Hematology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
David W EssexSol Sherry Thrombosis Center, Department of Medicine/Hematology, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, USA.
Temple University · US

Funding

Functional Role of Protein Disulfide Isomerase Isoforms in PlateletsR01HL118526 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI ESSEX, DAVID W · 2013 to 2021
$4.4M
NHLBI NIH HHS R01 HL118526NIH HHS R01HL118526
6 · The paper itself

Abstract

There has recently been considerable progress of the field of extracellular protein disulfide isomerases with vascular thiol isomerases in the forefront. Four members of protein disulfide isomerase (PDI) family of enzymes, PDI, ERp57, ERp72, and ERp5, have been shown to be secreted from activated platelets and endothelial cells at the site of vascular injury. Each isomerase individually supports platelet accumulation and coagulation, as indicated by multiple levels of evidence, including inhibitory antibodies, targeted knockout mice, and mutant isomerases. The transmembrane PDI family member TMX1 was recently shown to inhibit platelet function and thrombosis, demonstrating that the PDIs can have opposing functions in thrombosis. These observations provide a new concept that thiol isomerases can both positively and negatively regulate hemostasis, constituting off-on redox switches controlling activation of hemostatic factors. This redox network serves to maintain vascular homeostasis. Integrins such as the αIIbβ3 fibrinogen receptor on platelets appear to be major substrates, with the platelet receptor for von Willebrand factor, glycoprotein Ibα, as another substrate. S-nitrosylation of the prothrombotic PDIs may additionally negatively regulate platelets and thrombosis. Thiol isomerases also regulate coagulation in mouse models, and a clinical trial with the oral PDI inhibitor isoquercetin substantially decreased markers of coagulation in patients at risk for thrombosis. This review updates recent findings in the field and addresses emerging evidence that thiol/disulfide-based reactions mediated by the prothrombotic secreted PDIs are balanced by the transmembrane member of this family, TMX1.

Indexed as

Sulfhydryl CompoundsThrombosisAnimalsBlood PlateletsEndothelial CellsHumansMicePlatelet Glycoprotein GPIIb-IIIa ComplexProtein Disulfide-IsomerasesPlatelet Glycoprotein GPIIb-IIIa ComplexProtein Disulfide-IsomerasesSulfhydryl Compoundsdisulfideintegrinplateletprotein disulfide isomerasesulfydrylthrombosis

Identifiers

PMID32702157
PMCPMC10496414
OpenAlexW3044994089

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.