Evidence map›Paper›PMID 36330424›Full record

ArticleFrontiers in neurology2022

Impairment of muscular endothelial cell regeneration in dermatomyositis.

D Lemmer, J Schmidt, K Kummer, B Lemmer, A Wrede, C Seitz, P Balcarek, K Schwarze, G A Müller, D Patschan and 1 more

Abstract read
In one paragraph

Article in Frontiers in neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

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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

11 authors.

D LemmerDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany.
J SchmidtDepartment of Neurology and Pain Treatment, Immanuel Klinik Rüdersdorf, University Hospital of the Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany.
K KummerDepartment of Neurology, Neuromuscular Center, University Medical Center Göttingen, Göttingen, Germany.
B LemmerDepartment of Physics, Georg-August-University Göttingen, Göttingen, Germany.
A WredeDepartment of Neuropathology, University Medical Center Göttingen, Göttingen, Germany.
C SeitzDepartment of Dermatology, Allergology and Venereology, University Medical Center Göttingen, Göttingen, Germany.
P BalcarekDepartment of Trauma Surgery, Orthopedics and Plastic Surgery, University Medical Center Göttingen, Göttingen, Germany.
K SchwarzeDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany.
G A MüllerDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany.
D PatschanFaculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany.
S PatschanFaculty of Health Sciences Brandenburg, Brandenburg Medical School Theodor Fontane, Rüdersdorf bei Berlin, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background and aim: Inflammatory myopathies are heterogeneous in terms of etiology, (immuno)pathology, and clinical findings. Endothelial cell injury, as it occurs in DM, is a common feature of numerous inflammatory and non-inflammatory vascular diseases. Vascular regeneration is mediated by both local and blood-derived mechanisms, such as the mobilization and activation of so-called proangiogenic cells (PACs) or early endothelial progenitor cells (eEPCs). The current study aimed to evaluate parameters of eEPC integrity in dermatomyositis (DM), compared to necrotizing myopathy (NM) and to non-myopathic controls. Methods: Blood samples from DM and NM patients were compared to non-myositis controls and analyzed for the following parameters: circulating CD133 Results: Seventeen (17) DM patients, 7 NM patients, and 40 non-myositis controls were included. CD133 Conclusion: Our study demonstrates the loss of intramuscular microvessels in DM, accompanied by endothelial activation in DM and NM. Vascular regeneration was impaired in DM and NM. The findings suggest a role for inflammation-associated vascular damage in the pathogenesis of DM.

Indexed as

angiogenic mediatorsendothelial (dys) functionmyositis - etiologyprogenitor cellsregeneration

Identifiers

PMID36330424
PMCPMC9623165

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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.