Evidence map›Paper›PMID 33258989›Full record

ArticleBasic research in cardiology2020

Platelet-derived calpain cleaves the endothelial protease-activated receptor 1 to induce vascular inflammation in diabetes.

Anastasia Kyselova, Amro Elgheznawy, Ilka Wittig, Juliana Heidler, Alexander W Mann, Wolfram Ruf, Ingrid Fleming, Voahanginirina Randriamboavonjy

Open access · hybridAbstract read
In one paragraph

Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Anastasia KyselovaInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, 60596, Frankfurt am Main, Germany.
Amro ElgheznawyInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, 60596, Frankfurt am Main, Germany.
Ilka WittigGerman Center for Cardiovascular Research (DZHK), Partner site Rhein-Main, Frankfurt am Main, Germany.
Juliana HeidlerGerman Center for Cardiovascular Research (DZHK), Partner site Rhein-Main, Frankfurt am Main, Germany.
Alexander W MannEndokrinologikum Frankfurt, 60596, Frankfurt am Main, Germany.
Wolfram RufGerman Center for Cardiovascular Research (DZHK), Partner site Rhein-Main, Frankfurt am Main, Germany.
Ingrid FlemingInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, 60596, Frankfurt am Main, Germany.
Voahanginirina RandriamboavonjyInstitute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Theodor-Stern-Kai 7, 60596, Frankfurt am Main, Germany. voahangy@vrc.uni-frankfurt.de.ORCID 0000-0002-3542-6672
Goethe University Frankfurt · DEEndokrinologikum · DEScripps Research Institute · US

Funding

Deutsche Forschungsgemeinschaft EXC 2026, Project ID: 390649896Deutsche Forschungsgemeinschaft RA 2435/3-1Deutsche Forschungsgemeinschaft SFB 815/A16Deutsche Forschungsgemeinschaft SFB 815/Z1
6 · The paper itself

Abstract

Diabetes mellitus is a major risk factor for cardiovascular disease. Platelets from diabetic patients are hyperreactive and release microparticles that carry activated cysteine proteases or calpains. Whether platelet-derived calpains contribute to the development of vascular complications in diabetes is unknown. Here we report that platelet-derived calpain1 (CAPN1) cleaves the protease-activated receptor 1 (PAR-1) on the surface of endothelial cells, which then initiates a signaling cascade that includes the activation of the tumor necrosis factor (TNF)-α converting enzyme (TACE). The latter elicits the shedding of the endothelial protein C receptor and the generation of TNF-α, which in turn, induces intracellular adhesion molecule (ICAM)-1 expression to promote monocyte adhesion. All of the effects of CAPN1 were mimicked by platelet-derived microparticles from diabetic patients or from wild-type mice but not from CAPN1

Indexed as

ADAM17 ProteinAdultAnimalsBlood PlateletsCalpainCase-Control StudiesCell-Derived MicroparticlesCells, CulturedDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic AngiopathiesEndothelial CellsEndothelial Protein C ReceptorFemaleHumansIntercellular Adhesion Molecule-1ADAM17 ProteinCalpainCAPN1 protein, humanCapn1 protein, mouseEndothelial Protein C ReceptorIntercellular Adhesion Molecule-1Receptor, PAR-1Tumor Necrosis Factor-alphaCalpainEndothelial cellsEndothelial protein C receptorICAM-1Microparticles

Identifiers

PMID33258989
PMCPMC7716944
OpenAlexW3109453709

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.