Evidence map›Paper›PMID 27327039›Full record

ReviewJournal of vascular research2016

Multidimensional Contribution of Matrix Metalloproteinases to Atherosclerotic Plaque Vulnerability: Multiple Mechanisms of Inhibition to Promote Stability.

Jean Marie Ruddy, John S Ikonomidis, Jeffrey A Jones

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of vascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

29 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Role of oncostatin-M in ECM remodeling and plaque vulnerability.Molecular and cellular biochemistry · 2023
    Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. CircRNA-miRNA interactions in atherogenesis.Molecular and cellular biochemistry · 2022
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Altered Vascular Extracellular Matrix in the Pathogenesis of Atherosclerosis.Journal of cardiovascular translational research · 2021
    Review
  19. Statins Mitigate Stress-Related Vascular Aging and Atherosclerosis inFrontiers in cell and developmental biology · 2021
    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

3 authors at 1 institution in 1 country.

Jean Marie RuddyDivision of Vascular Surgery, Department of Surgery, Medical University of South Carolina, Charleston, S.C., USA.
John S Ikonomidis
Jeffrey A Jones
Medical University of South Carolina · US

Funding

Transmembrane Proteolytic Induction and Thoracic AneurysmsR01HL102121 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI IKONOMIDIS, JOHN S · 2011 to 2019
$3.0M
Extracellular Mechanisms For Thoracic Aortic AneurysmsR01HL075488 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI IKONOMIDIS, JOHN S · 2004 to 2008
$1.6M
Age-Dependent Mechanisms in Thoracic Aortic AneurysmsR01AG036954 · NIA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI IKONOMIDIS, JOHN S · 2011 to 2015
$1.5M
Transforming Growth Factor-beta Signaling Pathways in Thoracic Aortic AneurysmsI01BX000904 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI JONES, JEFFREY A. · 2011 to 2023
–
BLRD VA I01 BX000904NHLBI NIH HHS R01 HL075488NHLBI NIH HHS R01 HL102121NIA NIH HHS R01 AG036954
6 · The paper itself

Abstract

The prevalence of atherosclerotic disease continues to increase, and despite significant reductions in major cardiovascular events with current medical interventions, an additional therapeutic window exists. Atherosclerotic plaque growth is a complex integration of cholesterol penetration, inflammatory cell infiltration, vascular smooth muscle cell (VSMC) migration, and neovascular invasion. A family of matrix-degrading proteases, the matrix metalloproteinases (MMPs), contributes to all phases of vascular remodeling. The contribution of specific MMPs to endothelial cell integrity and VSMC migration in atherosclerotic lesion initiation and progression has been confirmed by the increased expression of these proteases in plasma and plaque specimens. Endogenous blockade of MMPs by the tissue inhibitors of metalloproteinases (TIMPs) may attenuate proteolysis in some regions, but the progression of matrix degeneration suggests that MMPs predominate in atherosclerotic plaque, precipitating vulnerability. Plaque neovascularization also contributes to instability and, coupling the known role of MMPs in angiogenesis to that of atherosclerotic plaque growth, interest in targeting MMPs to facilitate plaque stabilization continues to accumulate. This article aims to review the contributions of MMPs and TIMPs to atherosclerotic plaque expansion, neovascularization, and rupture vulnerability with an interest in promoting targeted therapies to improve plaque stabilization and decrease the risk of major cardiovascular events.

Indexed as

Angiogenesis InhibitorsAnimalsArteriesAtherosclerosisBiomarkersDisease ProgressionDrug DesignHumansMatrix Metalloproteinase InhibitorsMatrix MetalloproteinasesMicroRNAsMolecular Targeted TherapyNeovascularization, PathologicRupture, SpontaneousTissue Inhibitor of MetalloproteinasesAngiogenesis InhibitorsBiomarkersMatrix Metalloproteinase InhibitorsMatrix MetalloproteinasesMicroRNAsTissue Inhibitor of Metalloproteinases

Identifiers

PMID27327039
PMCPMC7196926
OpenAlexW2466123288

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.