Evidence map›Paper›PMID 32861744›Full record

ReviewCellular signalling2020

The multifaceted role of plasminogen in inflammation.

Beate Heissig, Yousef Salama, Satoshi Takahashi, Taro Osada, Koichi Hattori

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular signalling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 2% 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

69 citing papers in PubMed, 2 syntheses or guidelines pooled it, 112 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Enolase-1 and Inflammation.Biomolecules · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Role of Clot Formation and Plasminogen Activation in Lower Urinary Tract Pathologies.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

9 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

5 authors at 4 institutions in 2 countries.

Beate HeissigDepartment of Immunological Diagnosis, Juntendo University, School of Medicine, 2-1-1 Hongo, Bunkyo-Ku, Tokyo 113-8421, Japan. Electronic address: heissig@juntendo.ac.jp.
Yousef SalamaAn-Najah Center for Cancer and Stem Cell Research, Faculty of Medicine and Health Sciences, An-Najah National University, Nablus, Palestine. Electronic address: yousef.ut@najah.edu.
Satoshi TakahashiDepartment of Hematology, The Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan. Electronic address: radius@ims.u-tokyo.ac.jp.
Taro OsadaDepartment of Gastroenterology, Juntendo University Urayasu Hospital, 2-1-1 Tomioka, Urayasu-shi, 279-0021 Chiba, Japan. Electronic address: otaro@juntendo.ac.jp.
Koichi HattoriCenter for Genomic & Regenerative Medicine, Juntendo University, School of Medicine, 2-1-1 Hongo, Bunkyo-Ku, Tokyo 113-8421, Japan. Electronic address: khattori@ims.u-tokyo.ac.jp.
Juntendo University · JPAn-Najah National University · PSJuntendo University Urayasu Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A fine-tuned activation and deactivation of proteases and their inhibitors are involved in the execution of the inflammatory response. The zymogen/proenzyme plasminogen is converted to the serine protease plasmin, a key fibrinolytic factor by plasminogen activators including tissue-type plasminogen activator (tPA). Plasmin is part of an intricate protease network controlling proteins of initial hemostasis/coagulation, fibrinolytic and complement system. Activation of these protease cascades is required to mount a proper inflammatory response. Although best known for its ability to dissolve clots and cleave fibrin, recent studies point to the importance of fibrin-independent functions of plasmin during acute inflammation and inflammation resolution. In this review, we provide an up-to-date overview of the current knowledge of the enzymatic and cytokine-like effects of tPA and describe the role of tPA and plasminogen receptors in the regulation of the inflammatory response with emphasis on the cytokine storm syndrome such as observed during coronavirus disease 2019 or macrophage activation syndrome. We discuss tPA as a modulator of Toll like receptor signaling, plasmin as an activator of NFkB signaling, and summarize recent studies on the role of plasminogen receptors as controllers of the macrophage conversion into the M2 type and as mediators of efferocytosis during inflammation resolution.

Indexed as

AnimalsBlood CoagulationComplement ActivationCoronavirus InfectionsCOVID-19Cytokine Release SyndromeCytokinesHumansImmune SystemInflammationLow Density Lipoprotein Receptor-Related Protein-1NF-kappa BPandemicsPlasminogenPneumonia, ViralTissue Plasminogen ActivatorCytokinesLow Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanNF-kappa BPlasminogenTissue Plasminogen ActivatorCoagulationComplementCOVID-19CytokineCytokine storm syndromeDICLRP1Macrophage activation syndromeMatrix metalloproteinaseNFkBPARPlasminPlasminogenPlasminogen receptorToll like recepotortPA

Identifiers

PMID32861744
PMCPMC7452830
OpenAlexW3080387666

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.