Evidence map›Paper›PMID 36675310›Full record

ReviewInternational journal of molecular sciences2023

The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression.

Yosuke Kanno

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
12.9field-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

47 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Peptide Angio-3 Attenuates Pulmonary Fibrosis Via Modulation of the Coagulation Factor Xa-Protease-Activated Receptor-1 Signaling Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  5. Article
  6. Beyond Fibrinolysis: Urokinase Plasminogen Activator as an Early Regulator of Obesity.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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  8. Review
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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.

Yosuke KannoDepartment of Clinical Pathological Biochemistry, Faculty of Pharmaceutical Science, Doshisha Women's College of Liberal Arts, Kyoto 610-0395, Japan.ORCID 0000-0001-9741-2113
Doshisha Women's College of Liberal Arts · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrotic diseases, such as systemic sclerosis (SSc), idiopathic pulmonary fibrosis, renal fibrosis and liver cirrhosis are characterized by tissue overgrowth due to excessive extracellular matrix (ECM) deposition. Fibrosis progression is caused by ECM overproduction and the inhibition of ECM degradation due to several events, including inflammation, vascular endothelial dysfunction, and immune abnormalities. Recently, it has been reported that urokinase plasminogen activator (uPA) and its receptor (uPAR), known to be fibrinolytic factors, orchestrate the inflammatory response, vascular homeostasis, and immune homeostasis system. The uPA/uPAR system may show promise as a potential therapeutic target for fibrotic diseases. This review considers the role of the uPA/uPAR system in the progression of fibrotic diseases.

Indexed as

InflammationUrokinase-Type Plasminogen ActivatorFibrosisHomeostasisHumansImmune SystemUrokinase-Type Plasminogen Activatorfibrosis 23plasminuPAuPAR

Identifiers

PMID36675310
PMCPMC9866279
OpenAlexW4316672761

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.