Evidence map›Paper›PMID 25091012›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2014

Complement protein C1q promotes macrophage anti-inflammatory M2-like polarization during the clearance of atherogenic lipoproteins.

Weston Spivia, Patrick S Magno, Patrick Le, Deborah A Fraser

Open access · greenAbstract read
In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2014. 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
1.7field-weighted citation impact, top 17% 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

51 citing papers in PubMed, 80 citations in OpenAlex.

  1. Role of HMGB1 in Neuroinflammation.Molecular neurobiology · 2026
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  12. Complement system activation in wild boar (Frontiers in veterinary science · 2025
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  16. The frequency of CD38Nature communications · 2024
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  20. Observational
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

4 authors at 1 institution in 1 country.

Weston SpiviaDepartment of Biological Sciences, California State University Long Beach, 1250 Bellflower Blvd, Long Beach, CA, 90840, USA.
Patrick S Magno
Patrick Le
Deborah A Fraser
California State University, Long Beach · US

Funding

Research Initiative for Scientific Enhancement at CSULBR25GM071638 · NIGMS · CALIFORNIA STATE UNIVERSITY LONG BEACH · PI BUONORA, PAUL T, FRASER, DEBORAH ANN · 2004 to 2022
$10.0M
NIGMS NIH HHS 5R25GM071638NIGMS NIH HHS R25 GM071638
6 · The paper itself

Abstract

objectiveInnate immune protein C1q plays a dual role in the chronic inflammatory disease of atherosclerosis. Complement activation via C1q exacerbates pathology in the atherosclerotic lesion in later stages of the disease. However, in early stages of disease C1q is protective. We hypothesize that complement-independent activities of C1q are involved in reprogramming macrophage inflammatory polarization.

methodsThe influence of C1q on macrophage inflammatory responses during clearance of oxLDL was examined. Changes in cytokines at the gene and protein level were measured by quantitative PCR and ELISA assay.

resultsC1q modulated cytokine expression in Raw264.7 macrophages during ingestion of oxLDL. Levels of pro-inflammatory cytokines IL-1β and IL-6 were downregulated by C1q, whereas levels of the anti-inflammatory cytokine IL-10 were increased. In addition, data from an NFκB-luciferase gene reporter assay suggest that C1q suppresses activation of NFκB during lipoprotein clearance in macrophages, providing one mechanism by which C1q downregulates pro-inflammatory cytokine production.

conclusionsC1q-polarization of macrophages toward an anti-inflammatory (M2-like) phenotype may be important in dampening inflammation in the early atherosclerotic lesion. Further investigation of molecular pathways targeted by C1q may provide novel therapeutic targets for this disease.

Indexed as

AnimalsAtherosclerosisCell LineCells, CulturedComplement C1qCytokinesLipoproteins, LDLMacrophagesMiceMice, Inbred C57BLNF-kappa BComplement C1qCytokinesLipoproteins, LDLNF-kappa B

Identifiers

PMID25091012
PMCPMC5154336
OpenAlexW1973534951

What OpenQuestion holds

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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.