Evidence map›Paper›PMID 25027488›Full record

ReviewNature reviews. Cardiology2014

The role of heat shock proteins in atherosclerosis.

Georg Wick, Bojana Jakic, Maja Buszko, Marius C Wick, Cecilia Grundtman

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
7.3field-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

81 citing papers in PubMed, 165 citations in OpenAlex.

  1. Article
  2. Article
  3. CD8Nature reviews. Cardiology · 2026
    Review
  4. Review
  5. Review
  6. An antigen-less pro-vaccine for treating autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2025
    Article
  7. Benzene metabolites increase vascular permeability by activating heat shock proteins and Rho GTPases.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  8. Review
  9. Article
  10. Promising Adventitia in Atherosclerosis.Current vascular pharmacology · 2025
    Review
  11. Article
  12. The role of HSP40 in cancer: Recent advances.Histology and histopathology · 2024
    Review
  13. Review
  14. Article
  15. Atherosclerosis antigens as targets for immunotherapy.Nature cardiovascular research · 2023
    Review
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review

21 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

5 authors at 1 institution in 1 country.

Georg WickLaboratory of Autoimmunity, Section for Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr-Strasse 1a, 6020 Innsbruck, Austria.
Bojana JakicLaboratory of Autoimmunity, Section for Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr-Strasse 1a, 6020 Innsbruck, Austria.
Maja BuszkoLaboratory of Autoimmunity, Section for Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr-Strasse 1a, 6020 Innsbruck, Austria.
Marius C WickDepartment of Radiology, Karolinska University Hospital, Karolinska Vägen, Solna 17176 Stockholm, Sweden.
Cecilia GrundtmanLaboratory of Autoimmunity, Section for Experimental Pathophysiology and Immunology, Biocenter, Innsbruck Medical University, Peter-Mayr-Strasse 1a, 6020 Innsbruck, Austria.
Innsbruck Medical University · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic, multifactorial disease that starts in youth, manifests clinically later in life, and can lead to myocardial infarction, stroke, claudication, and death. Although inflammatory processes have long been known to be involved in atherogenesis, interest in this subject has grown in the past 30-40 years. Animal experiments and human analyses of early atherosclerotic lesions have shown that the first pathogenic event in atherogenesis is the intimal infiltration of T cells at arterial branching points. These T cells recognize heat shock protein (HSP)60, which is expressed together with adhesion molecules by endothelial cells in response to classic risk factors for atherosclerosis. Although these HSP60-reactive T cells initiate atherosclerosis, antibodies to HSP60 accelerate and perpetuate the disease. All healthy humans develop cellular and humoral immunity against microbial HSP60 by infection or vaccination. Given that prokaryotic (bacterial) and eukaryotic (for instance, human) HSP60 display substantial sequence homology, atherosclerosis might be the price we pay for this protective immunity, if risk factors stress the vascular endothelial cells beyond physiological conditions.

Indexed as

AnimalsAtherosclerosisBiomarkersChaperonin 60Heat-Shock ProteinsHumansInflammationBiomarkersChaperonin 60Heat-Shock Proteins

Identifiers

PMID25027488
OpenAlexW2001767617

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.