Evidence map›Paper›PMID 21868698›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2011

Urokinase-type plasminogen activator deficiency in bone marrow-derived cells augments rupture of angiotensin II-induced abdominal aortic aneurysms.

Haruhito A Uchida, Aruna Poduri, Venkateswaran Subramanian, Lisa A Cassis, Alan Daugherty

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Novel pharmacological approaches in abdominal aortic aneurysm.Clinical science (London, England : 1979) · 2023
    Review
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  8. Aortic Aneurysms.Arteriosclerosis, thrombosis, and vascular biology · 2017
    Review
  9. Relaxin and Matrix Metalloproteinase-9 in Angiotensin II-Induced Abdominal Aortic Aneurysms.Circulation journal : official journal of the Japanese Circulation Society · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Haruhito A UchidaSaha Cardiovascular Research Center, University of Kentucky, Lexington, KY 40536-0509, USA.
Aruna Poduri
Venkateswaran Subramanian
Lisa A Cassis
Alan Daugherty
University of Kentucky · US

Funding

Specific Secretory Phospholipase A2 Isozymes Promote Aneurysm FormationP01HL080100 · NHLBI · UNIVERSITY OF KENTUCKY · PI CASSIS, LISA A · 2006 to 2010
$8.2M
NHLBI NIH HHS P01 HL080100NHLBI NIH HHS P01-HL80100
6 · The paper itself

Abstract

objectiveAbdominal aortic aneurysms (AAAs) are associated with fragmentation of extracellular matrix during development of aortic dilation and rupture. Therefore, it is important to identify specific protease systems involved in extracellular matrix degradation during AAA formation. The present study determined the contribution of the urokinase system to AAA formation and rupture. METHODS AND

resultsAngiotensin II (Ang II)-induced AAAs were associated with increased aortic abundance of both urokinase-type plasminogen activator receptor (uPAR) and urokinase-type plasminogen activator (uPA) proteins. However, this increased presence was unrelated to AAA formation because deficiencies of either uPAR or uPA had no effect on either the incidence or size of Ang II-induced AAAs in both normolipidemic mice and low-density lipoprotein receptor-/- mice fed a saturated fat-enriched diet. Although uPA deficiency did not affect development of AAAs, there was an effect of increasing mortality rate from AAA rupture in hypercholesterolemic mice. Bone marrow transplantation demonstrated that enhanced aneurysmal rupture was attributable to deficiency of uPA in leukocytes. uPA deficiency led to an increased propensity for impaired resolution of the thrombotic material within the aneurysmal tissue. Neither uPAR nor uPA deficiency had any effect on Ang II-induced atherosclerosis in low-density lipoprotein receptor-/- mice.

conclusionsThe uPA-uPAR axis has no effect on the formation of Ang II-induced AAAs, but uPA deficiency promotes aneurysmal rupture.

Indexed as

Aneurysm, RupturedAngiotensin IIAnimalsAortic Aneurysm, AbdominalApolipoproteins EBone Marrow CellsDisease Models, AnimalHypercholesterolemiaIncidenceLeukocytesMiceMice, Inbred C57BLMice, KnockoutReceptors, LDLReceptors, Urokinase Plasminogen ActivatorUrokinase-Type Plasminogen ActivatorAngiotensin IIApolipoproteins EReceptors, LDLReceptors, Urokinase Plasminogen ActivatorUrokinase-Type Plasminogen Activator

Identifiers

PMID21868698
PMCPMC3220732
OpenAlexW2076185523

What OpenQuestion holds

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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.