Evidence map›Paper›PMID 24944761›Full record

ReviewWorld journal of cardiology2014

Autoantibodies to apolipoprotein A-1 as a biomarker of cardiovascular autoimmunity.

Nicolas Vuilleumier, Fabrizio Montecucco, Oliver Hartley

Open access · hybridAbstract readReview
In one paragraph

Review in World journal of cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 28 citations in OpenAlex.

  1. CD8Nature reviews. Cardiology · 2026
    Review
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  12. ApoA1 and ApoA1-specific self-antibodies in cardiovascular disease.Laboratory investigation; a journal of technical methods and pathology · 2016
    Review
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 2 countries.

Nicolas VuilleumierNicolas Vuilleumier, Fabrizio Montecucco, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 1211 Geneva, Switzerland.
Fabrizio MontecuccoNicolas Vuilleumier, Fabrizio Montecucco, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 1211 Geneva, Switzerland.
Oliver HartleyNicolas Vuilleumier, Fabrizio Montecucco, Department of Genetics and Laboratory Medicine, Geneva University Hospitals, 1211 Geneva, Switzerland.
University Hospital of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immune-driven inflammation plays an important part in atherogenesis and is therefore believed to be key to the development of cardiovascular disease (CVD), which is currently the leading cause of death in the Western world. By fulfilling some of the Koch postulates, atherogenesis has even been proposed to be considered as an autoimmune disease, raising the hope that CVD could be prevented by immunomodulation. Nevertheless, the role of the immune system and autoimmune reactions in atherosclerosis appear to be a double edged-sword, with both pro-atherogenic and anti-atherogenic attributes. Hence, if immunomodulation is to become a therapeutic option for atherosclerosis and CVD, it will be crucial to correctly identify patients who might benefit from targeted suppression of deleterious autoimmune responses. This could be achieved, for example, by the detection of disease-associated autoantibodies. In this work, we will review the currently available clinical, in vitro, and animal studies dedicated to autoantibodies against apolipoprotein A-1 (anti-apoA-1 IgG), the major proteic fraction of high density lipoprotein. Current clinical studies indicate that high levels of anti-apoA-1 IgG are associated with a worse cardiovascular prognosis. In addition, in vitro and animal studies indicate a pro-inflammatory and pro-atherogenic role, supporting the hypothesis that these autoantibodies may play a direct causal role in CVD, and furthermore that they could potentially represent a therapeutic target for CVD in the future.

Indexed as

Apolipoprotein A-1AtherosclerosisAutoantibodiesAutoimmunityBiomarkersCardiovascular disease

Identifiers

PMID24944761
PMCPMC4062126
OpenAlexW1496777024

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.