Evidence map›Paper›PMID 40994550›Full record

ReviewFrontiers in molecular biosciences2025

The role of protease-activated receptors (PARs) in the functioning of platelets and platelet-derived microparticles (PMPs).

Urszula Jakobsche-Policht, Agnieszka Bronowicka-Szydełko, Rajmund Adamiec, Dorota Bednarska-Chabowska, Magdalena Mierzchała-Pasierb, Łukasz Lewandowski, Kinga Gostomska-Pampuch, Joanna Adamiec-Mroczek, Maciej Rabczyński, Edwin Kuźnik and 11 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in molecular biosciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Review
  3. 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

21 authors.

Urszula Jakobsche-PolichtDepartment of Angiology and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Agnieszka Bronowicka-SzydełkoDepartment of Biochemistry and Immunochemistry, Wroclaw Medical University, Wroclaw, Poland.
Rajmund AdamiecClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Dorota Bednarska-ChabowskaClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Magdalena Mierzchała-PasierbDepartment of Biochemistry and Immunochemistry, Wroclaw Medical University, Wroclaw, Poland.
Łukasz LewandowskiDepartment of Biochemistry and Immunochemistry, Wroclaw Medical University, Wroclaw, Poland.
Kinga Gostomska-PampuchDepartment of Biochemistry and Immunochemistry, Wroclaw Medical University, Wroclaw, Poland.
Joanna Adamiec-MroczekClinical Department of Ophthalmology, Wroclaw Medical University, Wroclaw, Poland.
Maciej RabczyńskiClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Edwin KuźnikClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Paweł LubienieckiClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Olgierd DróżdżClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Helena MartynowiczClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.
Anna KwiecieńDepartment of Basic Chemical Sciences, Wroclaw Medical University, Wroclaw, Poland.
Małgorzata StrzeleckaDepartment of Medicinal Chemistry, Wroclaw Medical University, Wroclaw, Poland.
Dawid RudkiewiczFaculty of Medicine, Wroclaw Medical University, Wroclaw Medical University, Wroclaw, Poland.
Marcin PiersiakFaculty of Medicine, Wroclaw Medical University, Wroclaw Medical University, Wroclaw, Poland.
Maciej ZiomekFaculty of Medicine, Wroclaw Medical University, Wroclaw Medical University, Wroclaw, Poland.
Mikołaj KondrackiFaculty of Medicine, Wroclaw Medical University, Wroclaw Medical University, Wroclaw, Poland.
Zuzanna GalińskaFaculty of Medicine, Wroclaw Medical University, Wroclaw Medical University, Wroclaw, Poland.
Katarzyna MadziarskaClinical Department of Diabetology, Hypertension and Internal Diseases, Institute of Internal Diseases, Wroclaw Medical University, Wroclaw, Poland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protease-activated receptors (PARs), present on the surface of platelets and platelet-derived microparticles (PMPs), belong to a superfamily of membrane receptors that play a key role in initiating intracellular G protein-dependent signaling pathways. Although four types of PARs have been identified-PAR-1, PAR-2, PAR-3, and PAR-4 - their mechanisms and functions remain poorly understood. Nevertheless, they are considered promising therapeutic and diagnostic targets, as they play crucial roles in initiating and promoting processes such as coagulation, inflammatory responses, and vascular function. PAR-1 is expressed on various cell types, including endothelial cells, platelets, neurons, and immune cells. Its activation by thrombin initiates a G protein-dependent signaling cascade that stimulates the expression of cytokines, selectins, adhesion molecules, and growth factors. In addition to thrombin, PAR-1 can also be activated by activated protein C (APC) and matrix metalloproteinase-1 (MMP-1). APC triggers cytoprotective signaling pathways, while MMP-1 influences cellular dynamics through alternative signaling mechanisms. PAR-1 activation is also affected by epigenetic modifications and genetic polymorphisms in the PAR-1 gene. Variants such as -1426 C/T and -506 I/D influence receptor expression and are associated with an increased risk of thrombosis, potentially due to epigenetic changes linked to atherosclerosis. The complex signaling network of PAR-1 makes it a promising therapeutic target for the treatment of cardiovascular diseases, cancer, and neuroinflammatory disorders. This paper serves as a compendium on PAR-1 and its role, particularly in the activation of platelets and PMPs.

Indexed as

atherosclerosishemostasisplatelet-derived microparticlesprotease-activated receptor (PAR-1)vessels

Identifiers

PMID40994550
PMCPMC12455044

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.