Evidence map›Paper›PMID 25364719›Full record

ReviewFrontiers in cell and developmental biology2014

Therapeutic potential of matrix metalloproteinases in Duchenne muscular dystrophy.

Yuji Ogura, Marjan M Tajrishi, Shuichi Sato, Sajedah M Hindi, Ashok Kumar

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Management and Outcomes of Femur Fractures in Patients with Duchenne Muscular Dystrophy.Journal of the Pediatric Orthopaedic Society of North America · 2023
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Biomarkers in Duchenne Muscular Dystrophy.Current heart failure reports · 2022
    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

5 authors at 1 institution in 1 country.

Yuji OguraDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine Louisville, KY, USA.
Marjan M TajrishiDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine Louisville, KY, USA.
Shuichi SatoDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine Louisville, KY, USA.
Sajedah M HindiDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine Louisville, KY, USA.
Ashok KumarDepartment of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine Louisville, KY, USA.
University of Louisville · US

Funding

TAK1/TRAF6 Signaling in Skeletal MuscleR01AR059810 · NIAMS · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2011 to 2021
$4.0M
Role of TWEAK in Skeletal Muscle MetabolismR01AG029623 · NIA · UNIVERSITY OF LOUISVILLE · PI KUMAR, ASHOK · 2007 to 2016
$2.8M
NIAMS NIH HHS R01 AR059810NIA NIH HHS R01 AG029623
6 · The paper itself

Abstract

Matrix metalloproteinases (MMPs) are secreted proteinases that have physiologic roles in degradation and remodeling of extracellular matrix (ECM) in almost all tissues. However, their excessive production in disease conditions leads to many pathological features including tissue breakdown, inflammation, cell death, and fibrosis. Duchenne Muscular dystrophy (DMD) is a devastating genetic muscle disorder caused by partial or complete loss of cytoskeletal protein dystrophin. Progressive muscle wasting in DMD is accompanied by myofiber necrosis followed by cycles of regeneration and degeneration and inflammation that eventually result in replacement of myofiber by connective and adipose tissues. Emerging evidence suggests that gene expression and the activity of various MMPs are aberrantly regulated in muscle biopsies from DMD patients and in skeletal muscle of animal models of DMD. Moreover, a few studies employing genetic mouse models have revealed that different MMPs play distinct roles in disease progression in DMD. Modulation of the activity of MMPs improves myofiber regeneration and enhances the efficacy of transplantation and engraftment of muscle progenitor cells in dystrophic muscle in mouse models of DMD. Furthermore, recent reports also suggest that some MMPs especially MMP-9 can serve as a biomarker for diagnosis and prognosis of DMD. In this article, we provide a succinct overview of the regulation of various MMPs and their therapeutic importance in DMD.

Indexed as

fibrosisinflammationmacrophagesmatrix metalloproteinasesNF-κBskeletal muscleTIMPs

Identifiers

PMID25364719
PMCPMC4207008
OpenAlexW2146872657

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.