Evidence map›Paper›PMID 31350818›Full record

ReviewArthritis & rheumatology (Hoboken, N.J.)2020

High-Density Lipoprotein in Lupus: Disease Biomarkers and Potential Therapeutic Strategy.

Sang Yeop Kim, Minzhi Yu, Emily E Morin, Jukyung Kang, Mariana J Kaplan, Anna Schwendeman

Open access · bronzeAbstract readReview
In one paragraph

Review in Arthritis & rheumatology (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
8.1field-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

49 citing papers in PubMed, 80 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Sang Yeop KimUniversity of Michigan, Ann Arbor.ORCID 0000-0002-5781-9039
Minzhi YuUniversity of Michigan, Ann Arbor.ORCID 0000-0002-3141-7285
Emily E MorinUniversity of Michigan, Ann Arbor.
Jukyung KangUniversity of Michigan, Ann Arbor.
Mariana J KaplanNational Institute of Arthritis and Musculoskeletal and Skin Diseases, NIH, Bethesda, Maryland.
Anna SchwendemanUniversity of Michigan, Ann Arbor.ORCID 0000-0002-8023-8080
University of Michigan · USNational Institute of Arthritis and Musculoskeletal and Skin Diseases · US

Funding

Systemic AutoimmunityZIAAR041199 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI KAPLAN, MARIANA · 2014 to 2025
$32.5M
Cellular Biotechnology Training Program (CBTP)T32GM008353 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SCHWENDEMAN, ANNA · 1991 to 2021
$9.3M
KLF14 and Cardiovascular DiseaseR01HL134569 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2017 to 2024
$5.3M
Synthetic HDL_a potential sepsis therapyR01GM113832 · NIGMS · UNIVERSITY OF KENTUCKY · PI LI, XIANG-AN, SCHWENDEMAN, ANNA · 2015 to 2019
$3.0M
Cellular Biotechnology Training Program (CBTP) - Years 31-35T32GM145304 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Guizhi Zhu · 2022 to 2026
$2.6M
Training Program in Translational Cardiovascular Research and EntrepreneurshipT32HL125242 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MICHELE, DANIEL E · 2015 to 2024
$1.9M
American Heart Association-American Stroke Association 19PRE34400017Intramural NIH HHS ZIA AR041199NHLBI NIH HHS R01 HL134569NHLBI NIH HHS T32 HL125242NIAMS NIH HHS ZIA AR041199NIGMS NIH HHS R01 GM113832NIGMS NIH HHS T32 GM008353NIGMS NIH HHS T32 GM145304NIH HHS R01 GM113832NIH HHS R01 HL134569
6 · The paper itself

Abstract

Systemic lupus erythematosus (SLE) patients exhibit accelerated development of atherosclerosis and increased incidents of cardiovascular disease (CVD) that cannot be explained by traditional risk factors alone. Accumulating evidence suggests that reduced levels of high-density lipoproteins (HDLs), along with altered HDL composition and function, may contribute to the accelerated atherosclerosis in SLE patients. Normally, HDLs play various atheroprotective roles through facilitating cholesterol efflux, inhibiting vascular inflammation, and scavenging oxidative species. However, systemic inflammation, oxidative stress, and autoimmunity in SLE patients induce changes in HDL size distribution and proteomic and lipidomic signatures. These compositional changes in HDLs result in the formation of proinflammatory, dysfunctional HDL. These lupus-altered HDLs have impaired antiatherogenic function with reduced cholesterol efflux capacities, impaired antioxidation abilities, and diminished antiinflammatory properties. In fact, dysfunctional HDL may promote atherogenesis by inducing inflammation. Thus, dysfunctional HDLs could be an important biomarker of accelerated atherosclerosis in lupus. Additionally, HDL-targeted therapies, especially infusion of reconstituted HDLs, may serve as a potential therapeutic intervention for SLE patients with CVD.

Indexed as

AtherosclerosisCholesterolCholesterol, HDLDyslipidemiasHumansInflammationLipoproteins, HDLLupus Erythematosus, SystemicOxidative StressCholesterolCholesterol, HDLLipoproteins, HDL

Identifiers

PMID31350818
PMCPMC6935404
OpenAlexW2965420943

What OpenQuestion holds

Textmetadata
LicenceTDM
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.