Evidence map›Paper›PMID 24618883›Full record

ArticleMolecular medicine (Cambridge, Mass.)2014

Increased expression and activation of absent in melanoma 2 inflammasome components in lymphocytic infiltrates of abdominal aortic aneurysms.

Susanne Dihlmann, Philipp Erhart, Arianeb Mehrabi, Arash Nickkholgh, Felix Lasitschka, Dittmar Böckler, Maani Hakimi

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. The role of absent in melanoma 2 (AIM2) in cardiovascular diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Review
  17. The diagnostic role of AIM2 in Kawasaki disease.Clinical and experimental medicine · 2021
    Article
  18. Structure, Activation and Regulation of NLRP3 and AIM2 Inflammasomes.International journal of molecular sciences · 2021
    Review
  19. Article
  20. 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

7 authors at 2 institutions in 1 country.

Susanne DihlmannDepartment of Vascular and Endovascular Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Philipp ErhartDepartment of Vascular and Endovascular Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Arianeb MehrabiDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Arash NickkholghDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Felix LasitschkaInstitute of Pathology, University Hospital Heidelberg, Heidelberg, Germany.
Dittmar BöcklerDepartment of Vascular and Endovascular Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Maani HakimiDepartment of Vascular and Endovascular Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Heidelberg University · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic vascular inflammation is a key hallmark in the pathogenesis of abdominal aortic aneurysm (AAA). Recent investigations have suggested that the inflammasome, a cytosolic multiprotein complex that recognizes pathogen-associated molecular patterns, plays a role in atherosclerosis. However, its role in AAA inflammation has not yet been investigated. This pilot study analyzed inflammasome activation and its intramural localization in 24 biopsy samples from 11 patients with asymptomatic AAA versus 12 aortic samples from apparently healthy controls. Using a histological inflammation scale, we identified grade 2/3 inflammatory changes with lymphoid aggregates/tertiary lymphoid organs in 21 out of 24 AAA samples, whereas only 7 of the 12 control samples exhibited local grade 1 inflammatory changes. Strong expression levels of "apoptosis-associated speck-like protein with a caspase recruitment domain" (ASC), caspase-1, caspase-5 and "absent in melanoma 2" (AIM2) were detected by immunohistochemistry in both sporadic infiltrating lymphoid cells and lymphoid aggregates located in the outer media and adventitia of AAA samples. In contrast, inflammasome-positive cells were restricted to cholesterol plaque-associated areas and to single infiltrating cells in control aortas. Analysis of gene expression using real-time polymerase chain reaction (PCR) revealed significantly increased median mRNA levels of the inflammasome core components PYCARD (ASC), CASP1 (Caspase-1) and IL1B (IL-1β) in AAA tissue compared with normal aorta. Moreover, significantly increased median amounts of AIM2 protein and mature caspase-5 (p20) were found in samples associated with high rupture risk compared with paired low rupture risk samples of the same AAA patient. We conclude from our data that AAA-associated lymphoid cells are capable of inflammasome signaling, suggesting that inflammasome activation is involved in the chronic inflammatory process driving AAA progression.

Indexed as

AgedAged, 80 and overAorta, AbdominalAortic Aneurysm, AbdominalCARD Signaling Adaptor ProteinsCaspase 1CaspasesCytoskeletal ProteinsDNA-Binding ProteinsFemaleHumansInflammasomesLymphocytesMaleMiddle AgedAIM2 protein, humanCARD Signaling Adaptor ProteinsCASP5 protein, humanCaspase 1CaspasesCytoskeletal ProteinsDNA-Binding ProteinsInflammasomesPYCARD protein, human

Identifiers

PMID24618883
PMCPMC4069270
OpenAlexW118944295

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.