Evidence map›Paper›PMID 31409673›Full record

ArticleBlood2019

Synergistic effects of ADAMTS13 deficiency and complement activation in pathogenesis of thrombotic microangiopathy.

Liang Zheng, Di Zhang, Wenjing Cao, Wen-Chao Song, X Long Zheng

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. ADAMTS13 in the New Era of TTP.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  19. A Simple, Robust, and Cost-effective Method for Genotyping Small-scale Mutations.Journal of clinical and translational pathology · 2022
    Article
  20. Observational
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

5 authors at 2 institutions in 1 country.

Liang ZhengDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL; and.
Di ZhangDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL; and.
Wenjing CaoDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL; and.
Wen-Chao SongDepartment of Systems Pharmacology and Translational Therapeutics, Perelman School of Medicine, The University of Pennsylvania, Philadelphia, PA.
X Long ZhengDivision of Laboratory Medicine, Department of Pathology, The University of Alabama at Birmingham, Birmingham, AL; and.ORCID 0000-0003-1680-5295
University of Alabama at Birmingham · USTranslational Therapeutics (United States) · US

Funding

Pathogenesis of Thrombotic MicroangiopathyR01HL126724 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI ZHENG, X. LONG · 2015 to 2018
$1.8M
Novel Therapeutics for Acquired Thrombotic Thrombocytopenic PurpuraR01HL144552 · NHLBI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ZHENG, X. LONG · 2019 to 2022
$1.8M
Mechanism underlying cofactor-dependent proteolysis of von Willebrand FactorR01HL157975 · NHLBI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ZHANG, XIAOHUI FRANK, ZHENG, X. LONG · 2022 to 2025
$1.8M
NHLBI NIH HHS R01 HL126724NHLBI NIH HHS R01 HL144552NHLBI NIH HHS R01 HL157975
6 · The paper itself

Abstract

Severe deficiency of plasma ADAMTS13 activity is the primary cause of thrombotic thrombocytopenic purpura (TTP) whereas overwhelming activation of complement via an alternative pathway results in atypical hemolytic uremic syndrome (aHUS), the prototypes of thrombotic microangiopathy (TMA). However, clinical and pathogenic distinctions between TTP and aHUS are often quite challenging. Clinical reports have suggested that complement activation may play a role in the development of TTP, which is caused by severe deficiency of plasma ADAMTS13 activity. However, the experimental evidence to support this hypothesis is still lacking. Here, we show that mice with either

Indexed as

Complement ActivationADAMTS13 ProteinAnimalsComplement Factor HGene DeletionMice, Inbred C57BLThrombotic MicroangiopathiesADAMTS13 ProteinADAMTS13 protein, mouseComplement Factor H

Identifiers

PMID31409673
PMCPMC6764266
OpenAlexW2968083681

What OpenQuestion holds

Textmetadata
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.