Evidence map›Paper›PMID 17638846›Full record

Trial reportBlood2007

Interferon-alpha promotes abnormal vasculogenesis in lupus: a potential pathway for premature atherosclerosis.

Michael F Denny, Seth Thacker, Hemal Mehta, Emily C Somers, Todd Dodick, Franck J Barrat, W Joseph McCune, Mariana J Kaplan

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 2 pooled it
6.8field-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

151 citing papers in PubMed, 2 syntheses or guidelines pooled it, 274 citations in OpenAlex.

  1. Pooled it
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  18. Residual Traditional Risk in Non-Traditional Atherosclerotic Diseases.International journal of molecular sciences · 2025
    Review
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  20. Review

91 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Michael F DennyDivision of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Seth Thacker
Hemal Mehta
Emily C Somers
Todd Dodick
Franck J Barrat
W Joseph McCune
Mariana J Kaplan
Center for Rheumatology · USDynavax Technologies (United States) · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
RESEARCH TRAINING IN EXPERIMENTAL IMMUNOPATHOLOGYT32AI007413 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Bethany B. Moore · 1993 to 2026
$9.8M
Vector CoreP30AR048310 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI FOX, DAVID A · 2001 to 2010
$5.9M
NETs in the development of lupus and its cardiovascular complicationsR01HL088419 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI EITZMAN, DANIEL T · 2009 to 2016
$3.1M
Mechanisms of T-cell induced-APC cytotoxicity in lupusK08AR048235 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAPLAN, MARIANA J · 2002 to 2006
$643k
NCI NIH HHS P30 CA046592NCI NIH HHS P30 CA46592NHLBI NIH HHS R01 HL088419NIAID NIH HHS T32-AI07413NIAMS NIH HHS AR048235NIAMS NIH HHS K08 AR048235NIAMS NIH HHS P30 AR048310NIAMS NIH HHS P30 AR48310
6 · The paper itself

Abstract

Individuals with systemic lupus erythematosus (SLE) have a striking increase in premature atherosclerosis of unclear etiology. Accelerated endothelial cell apoptosis occurs in SLE and correlates with endothelial dysfunction. Endothelial progenitor cells (EPCs) and myelomonocytic circulating angiogenic cells (CACs) are crucial in blood vessel repair after vascular damage, and decreased levels or abnormal function of EPCs/CACs are established atherosclerosis risk factors. We investigated if vascular repair is impaired in SLE. We report that SLE patients display abnormal phenotype and function of EPCs/CACs. These abnormalities are characterized by significant decreases in the number of circulating EPCs (310 +/- 50 EPCs/mL of blood in SLE versus 639 +/- 102 in controls) and significant impairments in the capacity of EPCs/CACs to differentiate into mature ECs and synthesize adequate levels of the proangiogenic molecules vascular endothelial growth factor (VEGF) and hepatic growth factor (HGF). These abnormalities are triggered by interferon-alpha (IFN-alpha), which induces EPC and CAC apoptosis and skews myeloid cells toward nonangiogenic phenotypes. Lupus EPCs/CACs have increased IFN-alpha expression and their supernatants promote higher induction of IFN-inducible genes. Importantly, neutralization of IFN pathways restores a normal EPC/CAC phenotype in lupus. SLE is characterized by an imbalance between endothelial cell damage and repair triggered by type I IFNs, which might promote accelerated atherosclerosis.

Indexed as

AdultApoptosisAtherosclerosisCell DifferentiationEndothelial CellsFemaleHumansInterferon-alphaLupus Erythematosus, SystemicMaleNeovascularization, PathologicReverse Transcriptase Polymerase Chain ReactionRNA, MessengerStem CellsInterferon-alphaRNA, Messenger

Identifiers

PMID17638846
PMCPMC2018671
OpenAlexW2151463001

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.