Evidence map›Paper›PMID 33262760›Full record

ReviewFrontiers in immunology2020

IFN-I Mediates Dysfunction of Endothelial Progenitor Cells in Atherosclerosis of Systemic Lupus Erythematosus.

Xuewei Ding, Wei Xiang, Xiaojie He

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

27 citing papers in PubMed, 42 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

3 authors at 2 institutions in 1 country.

Xuewei DingInstitute of Pediatrics, The Second Xiangya Hospital, Central South University, Changsha, China.
Wei XiangKey Laboratory of Tropical Translational Medicine of Ministry of Education, Hainan Medical University, NHC Key Laboratory of Control of Tropical diseases (Hainan Medical University), Haikou, China.
Xiaojie HeInstitute of Pediatrics, The Second Xiangya Hospital, Central South University, Changsha, China.
Second Xiangya Hospital of Central South University · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) is a multi-system autoimmune disease including the cardiovascular system. Atherosclerosis is the most common cardiovascular complication of SLE and a significant risk factor for morbidity and mortality. Vascular damage/protection mechanism in SLE patients is out of balance, caused by the cascade reaction among oxidative stress, proinflammatory cytokines, Neutrophil Extracellular Traps, activation of B cells and autoantibodies and abnormal T cells. As a precursor cell repairing vascular endothelium, endothelial progenitor cells (EPCs) belong to the protective mechanism and show the reduced number and impaired function in SLE. However, the pathological mechanism of EPCs dysfunction in SLE remains ill-defined. This paper reviews the latest SLE epidemiology and pathogenesis, discusses the changes in the number and function of EPCs in SLE, expounds the role of EPCs in SLE atherosclerosis, and provides new guidance and theoretical basis for exploring novel targets for SLE treatment.

Indexed as

AtherosclerosisAutoantibodiesB-LymphocytesCytokinesEndothelial Progenitor CellsExtracellular TrapsHumansInterferon Type ILupus Erythematosus, SystemicModels, ImmunologicalOxidative StressSignal TransductionT-LymphocytesAutoantibodiesCytokinesInterferon Type Iatherosclerosisendothelial cellendothelial progenitor cellIFN-Ipathogenesissystemic lupus erythematosus

Identifiers

PMID33262760
PMCPMC7686511
OpenAlexW3101713266

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.