Evidence map›Paper›PMID 33166409›Full record

ArticleBlood advances2020

Activated platelet-based inhibition of fibrinolysis via thrombin-activatable fibrinolysis inhibitor activation system.

Yuko Suzuki, Hideto Sano, Liina Mochizuki, Naoki Honkura, Tetsumei Urano

Open access · goldAbstract read
In one paragraph

Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.5field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Beyond Direct Fibrinolysis: Novel Approaches to Thrombolysis.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  3. Article
  4. Article
  5. Dependence of clot structure and fibrinolysis on apixaban and clotting activator.Research and practice in thrombosis and haemostasis · 2024
    Article
  6. Article
  7. Article
  8. Fibrinolysis: an illustrated review.Research and practice in thrombosis and haemostasis · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Group AFrontiers in cardiovascular medicine · 2021
    Article
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 1 institution in 1 country.

Yuko SuzukiDepartment of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hideto SanoDepartment of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Liina MochizukiDepartment of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Naoki HonkuraDepartment of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Tetsumei UranoDepartment of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Hamamatsu University School of Medicine · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Our previous real-time imaging studies directly demonstrated the spatiotemporal regulation of clot formation and lysis by activated platelets. In addition to their procoagulant functions, platelets enhanced profibrinolytic potential by augmenting the accumulation of tissue-type plasminogen activator (tPA) and plasminogen, in vivo in a murine microthrombus model, and in vitro in a platelet-containing plasma clot model. To clarify the role of thrombin-activatable fibrinolysis inhibitor (TAFI), which regulates coagulation-dependent anti-fibrinolytic potential, we analyzed tPA-induced clot lysis times in platelet-containing plasma. Platelets prolonged clot lysis times in a concentration-dependent manner, which were successfully abolished by a thrombomodulin-neutralizing antibody or an activated TAFI inhibitor (TAFIaI). The results obtained using TAFI- or factor XIII-deficient plasma suggested that TAFI in plasma, but not in platelets, was essential for this prolongation, though its cross-linkage with fibrin was not necessary. Confocal laser scanning microscopy revealed that fluorescence-labeled plasminogen accumulated on activated platelet surfaces and propagated to the periphery, similar to the propagation of fibrinolysis. Plasminogen accumulation and propagation were both enhanced by TAFIaI, but only accumulation was enhanced by thrombomodulin-neutralizing antibody. Labeled TAFI also accumulated on both fibrin fibers and activated platelet surfaces, which were Lys-binding-site-dependent and Lys-binding-site-independent, respectively. Finally, TAFIaI significantly prolonged the occlusion times of tPA-containing whole blood in a microchip-based flow chamber system, suggesting that TAFI attenuated the tPA-dependent prolongation of clot formation under flow. Thus, activated platelet surfaces are targeted by plasma TAFI, to attenuate plasminogen accumulation and fibrinolysis, which may contribute to thrombogenicity under flow.

Indexed as

Carboxypeptidase B2AnimalsBlood CoagulationBlood PlateletsFibrin Clot Lysis TimeFibrinolysisMiceCarboxypeptidase B2

Identifiers

PMID33166409
PMCPMC7656914
OpenAlexW3105217395

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.