Evidence map›Paper›PMID 31338604›Full record

ReviewCurrent rheumatology reports2019

Innate Immune Dysregulation in the Development of Cardiovascular Disease in Lupus.

Gantsetseg Tumurkhuu, Erica Montano, Caroline Jefferies

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current rheumatology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.1field-weighted citation impact, top 8% 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, 23 citations in OpenAlex.

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  13. Psoriasis and Connective Tissue Diseases.International journal of molecular sciences · 2020
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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 1 institution in 1 country.

Gantsetseg TumurkhuuDepartment of Medicine, Division of Rheumatology and Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Erica MontanoDepartment of Medicine, Division of Rheumatology and Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA.
Caroline JefferiesDepartment of Medicine, Division of Rheumatology and Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. caroline.jefferies@cshs.org.
Cedars-Sinai Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewThe systemic inflammatory nature of systemic lupus erythematosus (SLE) is patent not only in the diverse clinical manifestations of the disease but also in the increased risk of premature cardiovascular diseases (CVD). In this review, we discuss the latest findings on the key factors of the innate immune system known to play critical roles in the pathogenesis of accelerated CVD in patients with SLE and discuss the potential that immunometabolism may play a key role in this respect. RECENT

findingsRecent studies exploring the association between SLE and premature CVD clearly showed that alterations of specific immune functions play a pivotal role in the increased cardiovascular morbidity and mortality in the SLE patients. Novel molecular factors such as type I interferons (IFN), dysregulated neutrophil function, and changes to cellular metabolism and metabolites are emerging as important regulators of systemic immune dysfunction and as strong risk factors for premature CVD in SLE. Although corticosteroids and cytotoxic agents can be used to effectively manage and control various lupus-related complications, to date, no drug has been proven to prevent the development of premature atherosclerosis in SLE. However, as new mechanisms underlying this complication of SLE are uncovered, such as the role of metabolism and neutrophil-driven inflammation, new avenues for therapeutic intervention are being discovered.

Indexed as

AtherosclerosisCardiovascular DiseasesChemokine CCL2Endothelial CellsHumansImmunity, InnateInflammationInterferon Type ILeptinLupus Erythematosus, SystemicMacrophagesMetabolic SyndromeNeutrophilsReactive Oxygen SpeciesChemokine CCL2Interferon Type ILeptinReactive Oxygen SpeciesCardiovascular disease (CVD)LupusMetabolitesNETosisPBMCSystemic lupus erythematosus (SLE)Type I IFN

Identifiers

PMID31338604
OpenAlexW2964237006

What OpenQuestion holds

Textmetadata
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.