Evidence map›Paper›PMID 33669022›Full record

ArticleInternational journal of molecular sciences2021

Vascular Inflammation and Dysfunction in Lupus-Prone Mice-IL-6 as Mediator of Disease Initiation.

Paul Marczynski, Myriam Meineck, Ning Xia, Huige Li, Daniel Kraus, Wilfried Roth, Tamara Möckel, Simone Boedecker, Andreas Schwarting, Julia Weinmann-Menke

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Vascular damage in systemic lupus erythematosus.Nature reviews. Nephrology · 2024
    Review
  6. Article
  7. Review
  8. Not All Quiet on the Atherosclerosis Front.International journal of molecular sciences · 2023
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. 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

10 authors at 1 institution in 1 country.

Paul MarczynskiDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-9410-0525
Myriam MeineckDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Ning XiaInstitute of Pharmacology, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Huige LiInstitute of Pharmacology, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Daniel KrausDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.ORCID 0000-0002-6351-3706
Wilfried RothInstitute of Pathology, Medical Center of the Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Tamara MöckelDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Simone BoedeckerDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Andreas SchwartingDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Julia Weinmann-MenkeDepartment of Nephrology and Rheumatology, University Center of Autoimmunity, Johannes-Gutenberg University Mainz, 55131 Mainz, Germany.
Johannes Gutenberg University Mainz · DE

Funding

Deutsche Forschungsgemeinschaft ME3194/2-1; WE5779/4-1
6 · The paper itself

Abstract

backgroundSystemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease and patients are under an increased risk for cardiovascular (CV) events and mortality. The increased CV risk for patients with SLE seems to be caused by a premature and accelerated atherosclerosis, attributable to lupus-specific risk factors (i.e., increased systemic inflammation, altered immune status), apart from traditional CV risk factors. To date, there is no established experimental model to explore the pathogenesis of this increased CV risk in SLE patients.

methodsHere we investigated whether MRL-

resultsContrary to MRL-++ control mice, lupus-prone MRL-Faslpr mice exhibited a pronounced vascular and perivascular leukocytic infiltration in various organs; expression of pro-inflammatory cytokines in the aorta and kidney was augmented; and intima-media thickness of the aorta was increased. IL-6 deficiency reversed these changes and restored aortic relaxation.

conclusionOur findings demonstrate that the MRL-

Indexed as

AcetylcholineAnimalsAortaCytokinesDisease Models, AnimalEndothelium, VascularInflammationInterleukin-6KidneyLupus Erythematosus, SystemicLupus NephritisMacrophagesMiceMice, Inbred BALB CMice, KnockoutT-LymphocytesAcetylcholineCytokinesInterleukin-6interleukin-6, mouseTumor Necrosis Factor-alphaantibodycardiovascular diseasecytokinesIntima media thicknessmacrophagesystemic lupus erythematosusT Cells

Identifiers

PMID33669022
PMCPMC7956579
OpenAlexW3132140719

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.