Evidence map›Paper›PMID 18621108›Full record

ReviewNeuroscience2009

Diverse roles of matrix metalloproteinases and tissue inhibitors of metalloproteinases in neuroinflammation and cerebral ischemia.

E Candelario-Jalil, Y Yang, G A Rosenberg

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 274 papers.

0numbers the graph read from it
0cells of the map it votes in
274citing papers in PubMed
10.1field-weighted citation impact, top 2% 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

274 citing papers in PubMed, 513 citations in OpenAlex.

  1. Permeability imaging as a predictor of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Metabolic Endotoxemia: From the Gut to Neurodegeneration.International journal of molecular sciences · 2024
    Review

214 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

3 authors at 1 institution in 1 country.

E Candelario-JalilDepartment of Neurology, University of New Mexico Health Sciences Center, MSC10 5620, 1 University of New Mexico, Albuquerque, NM 87131-0001, USA.
Y Yang
G A Rosenberg
University of New Mexico · US

Funding

Pathobiology of Vascular Cognitive ImpairmentR01NS052305 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ROSENBERG, GARY ALLEN · 2006 to 2016
$4.3M
White matter hypoxia in a novel model of MMP-mediated inflammation in SHR/SPR01NS045847 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI ROSENBERG, GARY ALLEN · 2003 to 2017
$3.7M
NINDS NIH HHS R01 NS045847NINDS NIH HHS R01 NS052305
6 · The paper itself

Abstract

Regulation of the extracellular matrix by proteases and protease inhibitors is a fundamental biological process for normal growth, development and repair in the CNS. Matrix metalloproteinases (MMPs) and the tissue inhibitors of metalloproteinases (TIMPs) are the major extracellular-degrading enzymes. Two other enzyme families, a disintegrin and metalloproteinase (ADAM), and the serine proteases, plasminogen/plasminogen activator (P/PA) system, are also involved in extracellular matrix degradation. Normally, the highly integrated action of these enzyme families remodels all of the components of the matrix and performs essential functions at the cell surface involved in signaling, cell survival, and cell death. During the inflammatory response induced in infection, autoimmune reactions and hypoxia/ischemia, abnormal expression and activation of these proteases lead to breakdown of the extracellular matrix, resulting in the opening of the blood-brain barrier (BBB), preventing normal cell signaling, and eventually leading to cell death. There are several key MMPs and ADAMs that have been implicated in neuroinflammation: gelatinases A and B (MMP-2 and -9), stromelysin-1 (MMP-3), membrane-type MMP (MT1-MMP or MMP-14), and tumor necrosis factor-alpha converting enzyme (TACE). In addition, TIMP-3, which is bound to the cell surface, promotes cell death and impedes angiogenesis. Inhibitors of metalloproteinases are available, but balancing the beneficial and detrimental effects of these agents remains a challenge.

Indexed as

AnimalsAutoimmunityBlood-Brain BarrierBrain EdemaBrain IschemiaCell DeathEncephalitisExtracellular MatrixHumansMatrix MetalloproteinasesNerve DegenerationTissue Inhibitor of MetalloproteinasesMatrix MetalloproteinasesTissue Inhibitor of Metalloproteinases

Identifiers

PMID18621108
PMCPMC3584171
OpenAlexW2052322755

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.