Evidence map›Paper›PMID 33258804›Full record

ArticleThe Journal of clinical investigation2021

TREM-1 orchestrates angiotensin II-induced monocyte trafficking and promotes experimental abdominal aortic aneurysm.

Marie Vandestienne, Yujiao Zhang, Icia Santos-Zas, Rida Al-Rifai, Jeremie Joffre, Andreas Giraud, Ludivine Laurans, Bruno Esposito, Florence Pinet, Patrick Bruneval and 17 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Emerging Mechanisms of Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2026
    Review
  6. Article
  7. Efferocytosis-associated Mrc1Frontiers in immunology · 2026
    Article
  8. From inflammation to remodelling: A novel BASP1Journal of advanced research · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Myeloid Cells in Abdominal Aortic Aneurysm.Current atherosclerosis reports · 2025
    Review
  16. Article
  17. Tissue-resident CCR2Cell reports · 2025
    Article
  18. Article
  19. Article
  20. Article
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

27 authors at 3 institutions in 3 countries.

Marie VandestienneUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Yujiao ZhangUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Icia Santos-ZasUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Rida Al-RifaiUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Jeremie JoffreUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Andreas GiraudUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Ludivine LauransUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Bruno EspositoUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Florence PinetINSERM U1167-Institut Pasteur de Lille, Lille, France.
Patrick BrunevalUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Juliette RaffortUniversité Côte d'Azur, Centre Hospitalo-Universitaire (CHU), INSERM, C3M, Nice, France.
Fabien LareyreUniversité Côte d'Azur, Centre Hospitalo-Universitaire (CHU), INSERM, C3M, Nice, France.
Jose VilarUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Amir BoufenzerINOTREM SA, Nancy, France.
Lea GuyonnetUniversité de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.
Coralie GuerinUniversité de Paris, Innovative Therapies in Haemostasis, INSERM, F-75006, Paris, France.
Eric ClauserUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Jean-Sébastien SilvestreUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Sylvie LangCardiology Department, Hôpital Saint-Antoine, AP-HP, Sorbonne Université, Paris, France.
Laurie Soulat-DufourCardiology Department, Hôpital Saint-Antoine, AP-HP, Sorbonne Université, Paris, France.
Alain TedguiUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Ziad MallatUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Soraya TalebUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Alexandre BoissonnasSorbonne Université, INSERM, CNRS, Centre d'Immunologie et des Maladies Infectieuses Cimi-Paris, Paris, France.
Marc DeriveINOTREM SA, Nancy, France.
Giulia ChinettiUniversité Côte d'Azur, Centre Hospitalo-Universitaire (CHU), INSERM, C3M, Nice, France.
Hafid Ait-OufellaUniversité de Paris, Inserm U970, Paris-Cardiovascular Research Center, Paris, France.
Inserm · FRSorbonne Université · FRCentre National de la Recherche Scientifique · FR

Funding

British Heart Foundation CH/10/001/27642British Heart Foundation RG/15/11/31593
6 · The paper itself

Abstract

The triggering receptor expressed on myeloid cells 1 (TREM-1) drives inflammatory responses in several cardiovascular diseases but its role in abdominal aortic aneurysm (AAA) remains unknown. Our objective was to explore the role of TREM-1 in a mouse model of angiotensin II-induced (AngII-induced) AAA. TREM-1 expression was detected in mouse aortic aneurysm and colocalized with macrophages. Trem1 gene deletion (Apoe-/-Trem1-/-), as well as TREM-1 pharmacological blockade with LR-12 peptide, limited both AAA development and severity. Trem1 gene deletion attenuated the inflammatory response in the aorta, with a reduction of Il1b, Tnfa, Mmp2, and Mmp9 mRNA expression, and led to a decreased macrophage content due to a reduction of Ly6Chi classical monocyte trafficking. Conversely, antibody-mediated TREM-1 stimulation exacerbated Ly6Chi monocyte aorta infiltration after AngII infusion through CD62L upregulation and promoted proinflammatory signature in the aorta, resulting in worsening AAA severity. AngII infusion stimulated TREM-1 expression and activation on Ly6Chi monocytes through AngII receptor type I (AT1R). In human AAA, TREM-1 was detected and TREM1 mRNA expression correlated with SELL mRNA expression. Finally, circulating levels of sTREM-1 were increased in patients with AAA when compared with patients without AAA. In conclusion, TREM-1 is involved in AAA pathophysiology and may represent a promising therapeutic target in humans.

Indexed as

Angiotensin IIAnimalsAortic Aneurysm, AbdominalCell MovementGene DeletionHumansInterleukin-1betaMatrix Metalloproteinase 2MiceMice, Knockout, ApoEMonocytesTriggering Receptor Expressed on Myeloid Cells-1Tumor Necrosis Factor-alphaAngiotensin IIIL1B protein, mouseInterleukin-1betaMatrix Metalloproteinase 2Mmp2 protein, mouseTREM1 protein, mouseTriggering Receptor Expressed on Myeloid Cells-1Tumor Necrosis Factor-alphaCell migration/adhesionInflammationInnate immunityMonocytesVascular Biology

Identifiers

PMID33258804
PMCPMC7810476
OpenAlexW3109712183

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.