Evidence map›Paper›PMID 16636270›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

Immune dysregulation accelerates atherosclerosis and modulates plaque composition in systemic lupus erythematosus.

Aleksandar K Stanic, Charles M Stein, Adam C Morgan, Sergio Fazio, MacRae F Linton, Edward K Wakeland, Nancy J Olsen, Amy S Major

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing 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

51 citing papers in PubMed.

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  14. The role of B cells in atherosclerosis.Nature reviews. Cardiology · 2019
    Review
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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

8 authors.

Aleksandar K StanicDivision of Cardiovascular Medicine, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232-6300, USA.
Charles M Stein
Adam C Morgan
Sergio Fazio
MacRae F Linton
Edward K Wakeland
Nancy J Olsen
Amy S Major

Funding

Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
Building Interdisciplinary Research Careers in Women's HealthK12HD043483 · NICHD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARTMANN, KATHERINE E, MAJOR, AMY S · 2002 to 2023
$10.3M
FUNCTIONAL HIERARCHY OF REMNANT LIPOPROTEIN RECEPTORSR01HL057986 · NHLBI · VANDERBILT UNIVERSITY · PI FAZIO, SERGIO · 1998 to 2016
$6.2M
ROLE OF FATTY ACID BINDING PROTEINS IN ATHEROSCLEROSISR01HL065405 · NHLBI · VANDERBILT UNIVERSITY · PI LINTON, MACRAE F · 2000 to 2009
$4.0M
MACROPHAGE EXPRESSION OF APOAI AND ATHEROSCLEROSISR01HL065709 · NHLBI · VANDERBILT UNIVERSITY · PI FAZIO, SERGIO · 2000 to 2008
$3.2M
BONE MARROW TRANSPLANTION AND ATHEROSCLEROSISR01HL053989 · NHLBI · VANDERBILT UNIVERSITY · PI LINTON, MACRAE F · 1995 to 2003
$1.5M
NHLBI NIH HHS HL53989NHLBI NIH HHS HL57986NHLBI NIH HHS HL65405NHLBI NIH HHS HL65709NHLBI NIH HHS R01 HL053989NHLBI NIH HHS R01 HL057986NHLBI NIH HHS R01 HL065405NHLBI NIH HHS R01 HL065709NICHD NIH HHS 5 K12 HD043483-04NICHD NIH HHS K12 HD043483NIDDK NIH HHS DK59637-01NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Patients with systemic lupus erythematosus (SLE) have accelerated atherosclerosis. The underlying mechanisms are poorly understood, and investigations have been hampered by the absence of animal models that reflect the human condition of generalized atherosclerosis and lupus. We addressed this problem by transferring lupus susceptibility to low-density lipoprotein (LDL) receptor-deficient (LDLr-/-) mice, an established model of atherosclerosis, creating radiation chimeras with NZM2410-derived, lupus-susceptible, B6.Sle1.2.3 congenic or C57BL/6 control donors (LDLr.Sle and LDLr.B6, respectively). LDLr.Sle mice developed a lupus-like disease characterized by production of double-stranded DNA autoantibodies and renal disease. When fed a Western-type diet, LDLr.Sle chimeras had increased mortality and atherosclerotic lesions. The plaques of LDLr.Sle mice were highly inflammatory and contained more CD3+ T cells than controls. LDLr.Sle mice also had increased activation of CD4+ T and B cells and significantly higher antibody to oxidized LDL and cardiolipin. Collectively, these studies demonstrate that the lupus-susceptible immune system enhances atherogenesis and modulates plaque composition.

Indexed as

AtherosclerosisAnimalsAntibodies, AntiphospholipidBone Marrow TransplantationDietHumansImmune SystemLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, KnockoutPhenotypeRadiation ChimeraReceptors, LDLSpleenThymus GlandAntibodies, AntiphospholipidReceptors, LDL

Identifiers

PMID16636270
PMCPMC1459011

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.