Evidence map›Paper›PMID 21347430›Full record

ArticlePloS one2011

A local proinflammatory signalling loop facilitates adverse age-associated arterial remodeling.

Mingyi Wang, Gaia Spinetti, Robert E Monticone, Jing Zhang, James Wu, Liqun Jiang, Benjamin Khazan, Richard Telljohann, Edward G Lakatta

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

32 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. Age as a risk factor in vasculitis.Seminars in immunopathology · 2022
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Observational
  10. Proinflammation, profibrosis, and arterial aging.Aging medicine (Milton (N.S.W)) · 2020
    Review
  11. Article
  12. Article
  13. Inflammation as a mediator of arterial ageing.Experimental physiology · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. NADPH Oxidases and Mitochondria in Vascular Senescence.International journal of molecular sciences · 2018
    Review
  18. The Impact of Aging on Cardio and Cerebrovascular Diseases.International journal of molecular sciences · 2018
    Review
  19. Review
  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

9 authors at 2 institutions in 2 countries.

Mingyi WangLaboratory of Cardiovascular Science, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America. mingyiw@grc.nia.nih.gov
Gaia Spinetti
Robert E Monticone
Jing Zhang
James Wu
Liqun Jiang
Benjamin Khazan
Richard Telljohann
Edward G Lakatta
National Institutes of Health · USNational Institute on Aging · US

Funding

Progression of Arterial Aging: the Local MCP-1/MMP-2/TGF-beta 1 Signaling LoopZIAAG000240 · NIA · NATIONAL INSTITUTE ON AGING · PI WANG, MINGYI · 2009 to 2025
$4.6M
Intramural NIH HHS
6 · The paper itself

Abstract

backgroundThe coincidence of vascular smooth muscle cells (VSMC) infiltration and collagen deposition within a diffusely thickened intima is a salient feature of central arterial wall inflammation that accompanies advancing age. However, the molecular mechanisms involved remain undefined. METHODOLOGY/PRINCIPAL

findingsImmunostaining and immunoblotting of rat aortae demonstrate that a triad of proinflammatory molecules, MCP-1, TGF-β1, and MMP-2 increases within the aortic wall with aging. Exposure of VSMC isolated from 8-mo-old rats (young) to MCP-1 effects, via CCR-2 signaling, both an increase in TGF-β1 activity, up to levels of untreated VSMC from 30-mo-old (old) rats, and a concurrent increase in MMP-2 activation. Furthermore, exposure of young VSMC to TGF-β1 increases levels of MCP-1, and MMP-2 activation, to levels of untreated VSMC from old rats. This autocatalytic signaling loop that enhances collagen production and invasiveness of VSMC is effectively suppressed by si-MCP-1, a CCR2 antagonist, or MMP-2 inhibition. CONCLUSIONS/SIGNIFICANCE: Threshold levels of MCP-1, MMP-2, or TGF-β1 activity trigger a feed-forward signaling mechanism that is implicated in the initiation and progression of adverse age-associated arterial wall remodeling. Intervention that suppressed this signaling loop may potentially retard age-associated adverse arterial remodeling.

Indexed as

Signal TransductionAgingAnimalsAortaChemokine CCL2CollagenEnzyme ActivationGene Expression RegulationInflammationMaleMatrix Metalloproteinase 2Muscle, Smooth, VascularProtein TransportRatsReceptors, CCR2Transforming Growth Factor beta1Ccl2 protein, ratChemokine CCL2CollagenMatrix Metalloproteinase 2Receptors, CCR2Transforming Growth Factor beta1

Identifiers

PMID21347430
PMCPMC3035650
OpenAlexW2072072860

What OpenQuestion holds

Textmetadata
LicenceCC0
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.