Evidence map›Paper›PMID 25587650›Full record

ReviewAnnual review of medicine2015

ADAMTS13 and von Willebrand factor in thrombotic thrombocytopenic purpura.

X Long Zheng

Open access · bronzeAbstract readReview
In one paragraph

Review in Annual review of medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.

0numbers the graph read from it
0cells of the map it votes in
153citing papers in PubMed
9.4field-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

153 citing papers in PubMed, 259 citations in OpenAlex.

  1. Trial
  2. Hyperadhesive von Willebrand Factor Contributes to Pathogenesis of Preeclampsia.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
  3. A rapid ADAMTS13 activity assay using a portable readout device.Blood vessels, thrombosis & hemostasis · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Platelet Disorders and Medication Strategies.Thrombosis and haemostasis · 2026
    Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

93 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

1 author at 1 institution in 1 country.

X Long ZhengDepartment of Pathology and Laboratory Medicine, The Children's Hospital of Philadelphia and The University of Pennsylvania Perelman School of Medicine, Philadelphia, Pennsylvania 19104; email: zheng@email.chop.edu.
Children's Hospital of Philadelphia · US

Funding

Structural Correlates of Protease and Cofactor FunctionP01HL074124 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI KRISHNASWAMY, SRIRAM · 2003 to 2013
$17.6M
Structure and Function of ADAMTS13 MetalloproteaseR01HL079027 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI ZHENG, X. LONG · 2005 to 2009
$1.6M
Novel Therapeutics for Acquired Thrombotic Thrombocytopenic PurpuraR01HL115187 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHENG, X. LONG · 2013 to 2016
$1.6M
NHLBI NIH HHS P01 HL074124NHLBI NIH HHS P01HL-074124NHLBI NIH HHS R01 HL079027NHLBI NIH HHS R01HL-079027NHLBI NIH HHS R01 HL115187NHLBI NIH HHS R01HL-115187
6 · The paper itself

Abstract

Pathogenesis of thrombotic thrombocytopenic purpura (TTP) was a mystery for over half a century until the discovery of ADAMTS13. ADAMTS13 is primarily synthesized in the liver, and its main function is to cleave von Willebrand factor (VWF) anchored on the endothelial surface, in circulation, and at the sites of vascular injury. Deficiency of plasma ADAMTS13 activity (<10%) resulting from mutations of the ADAMTS13 gene or autoantibodies against ADAMTS13 causes hereditary or acquired (idiopathic) TTP. ADAMTS13 activity is usually normal or modestly reduced (>20%) in other forms of thrombotic microangiopathy secondary to hematopoietic progenitor cell transplantation, infection, and disseminated malignancy or in hemolytic uremic syndrome. Plasma infusion or exchange remains the initial treatment of choice to date, but novel therapeutics such as recombinant ADAMTS13 and gene therapy are under development. Moreover, ADAMTS13 deficiency has been shown to be a risk factor for the development of myocardial infarction, stroke, cerebral malaria, and preeclampsia.

Indexed as

ADAM ProteinsADAMTS13 ProteinAutoantibodiesGenetic TherapyHumansMutationPurpura, Thrombotic ThrombocytopenicRecombinant Proteinsvon Willebrand FactorADAM ProteinsADAMTS13 ProteinADAMTS13 protein, humanAutoantibodiesRecombinant Proteinsvon Willebrand Factorarterial thrombosisautoantibodiesautoimmune disordermetalloproteasemutationsrare hematological disease

Identifiers

PMID25587650
PMCPMC4599565
OpenAlexW2108318098

What OpenQuestion holds

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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.