Evidence map›Paper›PMID 30410107›Full record

ReviewNature reviews. Cardiology2019

The role of B cells in atherosclerosis.

Andrew P Sage, Dimitrios Tsiantoulas, Christoph J Binder, Ziad Mallat

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 182 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
182citing papers in PubMed, 2 pooled it
–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

182 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Cardiovascular events risk in patients with systemic autoimmune diseases: a prognostic systematic review and meta-analysis.Clinical research in cardiology : official journal of the German Cardiac Society · 2024
    Pooled it
  2. Pooled it
  3. Trial
  4. Trial
  5. Article
  6. Article
  7. Unveiling the B-cell conundrum in in-stent restenosis.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Metabolic and Inflammatory Mechanisms Driving Atrial Fibrillation.Annual review of pharmacology and toxicology · 2026
    Review
  12. Review
  13. Article
  14. Review
  15. ApoB-specific CD4Frontiers in immunology · 2026
    Review
  16. Review
  17. Article
  18. Observational
  19. Review
  20. Review

122 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

4 authors.

Andrew P SageDivision of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, UK. aps63@cam.ac.uk.
Dimitrios TsiantoulasDivision of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, UK.
Christoph J BinderDepartment of Laboratory Medicine, Medical University of Vienna, Vienna, Austria.
Ziad MallatDivision of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0003-0443-7878

Funding

British Heart Foundation FS/15/57/31557British Heart Foundation PG/15/76/31756
6 · The paper itself

Abstract

The cardiovascular system is subject to hyperlipidaemic, inflammatory, and pro-oxidant stressors. Over time, these factors drive prevalent chronic diseases, of which atherosclerosis is most prominent and accounts for the majority of deaths globally. Antibody-producing B cells perform a unique role in responses to stress, injury, and infection. The power, inducibility, and adaptability of the antibody repertoire require an equally complex range of control measures. Defects and chronic perturbations in these checkpoints lead to inappropriate antibody responses, which might have important roles in shaping the development and outcome of atherosclerotic disease. A unique aspect related to atherosclerosis is the prominent role of natural antibodies, specifically those binding to the oxidized epitopes that are abundant on modified lipoproteins and cellular debris. B cells control cellular immune responses through cell-cell contact, antigen presentation, and cytokine production, and thereby participate in systemic and local immune responses in atherosclerotic arteries. To date, both proatherogenic and antiatherogenic properties have been assigned to B cells, depending on subsets and how they are functionally targeted. For these reasons, a deeper understanding of how B cells influence atherosclerotic plaque development is being pursued with the hope of providing novel B cell-targeted interventions to prevent inflammation-driven cardiovascular events.

Indexed as

Plaque, AtheroscleroticAnimalsAtherosclerosisAutoimmunityB-Lymphocyte SubsetsDyslipidemiasHumansImmunotherapyPhenotypeReceptors, Antigen, B-CellSignal TransductionReceptors, Antigen, B-Cell

Identifiers

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.