Evidence map›Paper›PMID 20088827›Full record

ArticleClinical science (London, England : 1979)2010

Angiotensin II infusion promotes ascending aortic aneurysms: attenuation by CCR2 deficiency in apoE-/- mice.

Alan Daugherty, Debra L Rateri, Israel F Charo, A Phillip Owens, Deborah A Howatt, Lisa A Cassis

Open access · hybridAbstract read
In one paragraph

Article in Clinical science (London, England : 1979), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
11.3field-weighted citation impact, top 1% 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

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 186 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Angiotensinogen as a Therapeutic Target for Cardiovascular and Metabolic Diseases.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  17. Article
  18. Phospholipase Cε insufficiency causes ascending aortic aneurysm and dissection.American journal of physiology. Heart and circulatory physiology · 2022
    Article
  19. Article
  20. Review

64 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

6 authors at 2 institutions in 1 country.

Alan DaughertySaha Cardiovascular Research Center, University of Kentucky, Lexington, KY 40536, U.S.A. Alan.Daugherty@uky.edu
Debra L Rateri
Israel F Charo
A Phillip Owens
Deborah A Howatt
Lisa A Cassis
University of Kentucky · USGladstone Institutes · US

Funding

Specific Secretory Phospholipase A2 Isozymes Promote Aneurysm FormationP01HL080100 · NHLBI · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2006 to 2010
$8.2M
STRUCTURE AND FUNCTION OF THE MONOCYTE MCP-1 RECEPTORR01HL052773 · NHLBI · J. DAVID GLADSTONE INSTITUTES · PI CHARO, ISRAEL F. · 1994 to 2010
$5.7M
NHLBI NIH HHS HL52773NHLBI NIH HHS HL80100NHLBI NIH HHS P01 HL080100NHLBI NIH HHS R01 HL052773
6 · The paper itself

Abstract

AngII (angiotensin II) induces atherosclerosis and AAAs (abdominal aortic aneurysms) through multiple proposed mechanisms, including chemotaxis. Therefore, we determined the effects of whole-body deficiency of the chemokine receptor CCR2 (CC chemokine receptor 2) on these diseases. To meet this objective, apoE (apolipoprotein E)-/- mice that were either CCR2+/+ or CCR2-/-, were infused with either saline or AngII (1000 ng.kg-1 of body weight.min-1) for 28 days via mini-osmotic pumps. Deficiency of CCR2 markedly attenuated both atherosclerosis and AAAs, unrelated to systolic blood pressure or plasma cholesterol concentrations. During the course of the present study, we also observed that AngII infusion led to large dilatations that were restricted to the ascending aortic region of apoE-/- mice. The aortic media in most of the dilated area was thickened. In regions of medial thickening, distinct elastin layers were discernable. There was an expansion of the distance between elastin layers in a gradient from the intimal to the adventitial aspect of the media. This pathology differed in a circumscribed area of the anterior region of ascending aortas in which elastin breaks were focal and almost transmural. All regions of the ascending aorta of AngII-infused mice had diffuse medial macrophage accumulation. Deficiency of CCR2 greatly attenuated the AngII-induced lumen dilatation in the ascending aorta. This new model of ascending aortic aneurysms has pathology that differs markedly from AngII-induced atherosclerosis or AAAs, but all vascular pathologies were attenuated by CCR2 deficiency.

Indexed as

Angiotensin IIAnimalsAortaAortic AneurysmApolipoproteins EBlood PressureBody WeightCholesterolDisease Models, AnimalHypercholesterolemiaLipidsMaleMiceMice, KnockoutReceptors, CCR2VasodilationAngiotensin IIApolipoproteins ECcr2 protein, mouseCholesterolLipidsReceptors, CCR2

Identifiers

PMID20088827
PMCPMC2841499
OpenAlexW1973423073

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.