Evidence map›Paper›PMID 35953533›Full record

ArticleScientific reports2022

Red blood cell distribution width is associated with increased interactions of blood cells with vascular wall.

Sharan Ananthaseshan, Krzysztof Bojakowski, Mariusz Sacharczuk, Piotr Poznanski, Dominik S Skiba, Lisa Prahl Wittberg, Jordan McKenzie, Anna Szkulmowska, Niclas Berg, Piotr Andziak and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
8.2field-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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 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

17 authors at 7 institutions in 3 countries.

Sharan AnanthaseshanDepartment of Medicine, Solna, Karolinska Institute, Stockholm, Sweden.
Krzysztof Bojakowski2nd Vascular Surgery and Angiology Department, Centre of Postgraduate Medical Education, Warsaw, Poland.
Mariusz SacharczukDepartment of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, 1a Banacha Street, 02-097, Warsaw, Poland.
Piotr PoznanskiDepartment of Experimental Genomics, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, Jastrzebiec, Poland.
Dominik S SkibaDepartment of Experimental Genomics, Institute of Genetics and Animal Biotechnology, Polish Academy of Sciences, Jastrzebiec, Poland.
Lisa Prahl WittbergKTH Mechanics, Royal Institute of Technology, Stockholm, Sweden.
Jordan McKenzieKTH Mechanics, Royal Institute of Technology, Stockholm, Sweden.
Anna SzkulmowskaAM2M Ltd. L.P., Torun, Poland.
Niclas BergKTH Mechanics, Royal Institute of Technology, Stockholm, Sweden.
Piotr Andziak2nd Vascular Surgery and Angiology Department, Centre of Postgraduate Medical Education, Warsaw, Poland.
Hanna MenkensDepartment of Medicine, Solna, Karolinska Institute, Stockholm, Sweden.
Maciej WojtkowskiInstitute of Physics, Nicolaus Copernicus University, Torun, Poland.
Dorota ReligaNVS, Karolinska Institute, Stockholm, Sweden.
Fredrik LundellKTH Mechanics, Royal Institute of Technology, Stockholm, Sweden.
Tomasz GuzikInstitute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, UK.
Zbigniew GaciongDepartment of Internal Medicine, Hypertension and Vascular Diseases, Medical University of Warsaw, 1a Banacha Street, 02-097, Warsaw, Poland. zgaciong@hotmail.com.
Piotr ReligaDepartment of Medicine, Solna, Karolinska Institute, Stockholm, Sweden.
KTH Royal Institute of Technology · SEKarolinska Institutet · SEMedical University of Warsaw · PLPolish Academy of Sciences · PLPostgraduate School of Molecular Medicine · PLNicolaus Copernicus University · PLUniversity of Glasgow · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanism underlying the association between elevated red cell distribution width (RDW) and poor prognosis in variety of diseases is unknown although many researchers consider RDW a marker of inflammation. We hypothesized that RDW directly affects intravascular hemodynamics, interactions between circulating cells and vessel wall, inducing local changes predisposing to atherothrombosis. We applied different human and animal models to verify our hypothesis. Carotid plaques harvested from patients with high RDW had increased expression of genes and proteins associated with accelerated atherosclerosis as compared to subjects with low RDW. In microfluidic channels samples of blood from high RDW subjects showed flow pattern facilitating direct interaction with vessel wall. Flow pattern was also dependent on RDW value in mouse carotid arteries analyzed with Magnetic Resonance Imaging. In different mouse models of elevated RDW accelerated development of atherosclerotic lesions in aortas was observed. Therefore, comprehensive biological, fluid physics and optics studies showed that variation of red blood cells size measured by RDW results in increased interactions between vascular wall and circulating morphotic elements which contribute to vascular pathology.

Indexed as

AtherosclerosisErythrocyte IndicesAnimalsBlood CellsCarotid ArteriesErythrocytesHumansMicePrognosisRisk Factors

Identifiers

PMID35953533
PMCPMC9366818
OpenAlexW4290805472

What Socratic 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 Socratic graph.