Evidence map›Paper›PMID 30216109›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

Genetic manipulation of CCN2/CTGF unveils cell-specific ECM-remodeling effects in injured skeletal muscle.

Jennifer M Petrosino, Andrew Leask, Federica Accornero

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.0field-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

34 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Drugs targeting CTGF in the treatment of pulmonary fibrosis.Journal of cellular and molecular medicine · 2024
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. CCN2 participates in overload-induced skeletal muscle hypertrophy.Matrix biology : journal of the International Society for Matrix Biology · 2022
    Article
  18. The mNature communications · 2022
    Article
  19. Article
  20. Volumetric compression develops noise-driven single-cell heterogeneity.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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 2 institutions in 2 countries.

Jennifer M PetrosinoDepartment of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
Andrew LeaskSchulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
Federica AccorneroDepartment of Physiology and Cell Biology, Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, USA.
The Ohio State University · USWestern University · CA

Funding

Post-transcriptional regulation of cardiac hypertrophyR01HL136951 · NHLBI · OHIO STATE UNIVERSITY · PI Federica Accornero · 2017 to 2026
$4.7M
Integrative Training in Biomedical SystemsT32GM068412 · NIGMS · OHIO STATE UNIVERSITY · PI PARVIN, JEFFREY D · 2005 to 2020
$2.4M
BEX1 and the control of protein translation in cardiac hypertrophyR00HL121284 · NHLBI · OHIO STATE UNIVERSITY · PI ACCORNERO, FEDERICA · 2016 to 2018
$727k
The role of BEX1 in translational control of muscle regeneration and reparative growthF31AR073638 · NIAMS · OHIO STATE UNIVERSITY · PI PETROSINO, JENNIFER MORGAN · 2018 to 2021
$139k
NHLBI NIH HHS R00 HL121284NHLBI NIH HHS R01 HL136951NIAMS NIH HHS F31 AR073638NIGMS NIH HHS T32 GM068412
6 · The paper itself

Abstract

In skeletal muscle, extracellular matrix (ECM) remodeling can either support the complete regeneration of injured muscle or facilitate pathologic fibrosis and muscle degeneration. Muscular dystrophy (MD) is a group of genetic disorders that results in a progressive decline in muscle function and is characterized by the abundant deposition of fibrotic tissue. Unlike acute injury, where ECM remodeling is acute and transient, in MD, remodeling persists until fibrosis obstructs the regenerative efforts of diseased muscles. Thus, understanding how ECM is deposited and organized is critical in the context of muscle repair. Connective tissue growth factor (CTGF or CCN2) is a matricellular protein expressed by multiple cell types in response to tissue injury. Although used as a general marker of fibrosis, the cell type-dependent role of CTGF in dystrophic muscle has not been elucidated. To address this question, a conditional Ctgf myofiber and fibroblast-knockout mouse lines were generated and crossed to a dystrophic background. Only myofiber-selective inhibition of CTGF protected δ-sarcoglycan-null ( Sgcd

Indexed as

Connective Tissue Growth FactorExtracellular MatrixGene Expression RegulationMuscle Fibers, SkeletalMuscular Dystrophy, AnimalAnimalsFibrosisMiceMice, KnockoutSarcoglycansCCN2 protein, mouseConnective Tissue Growth FactorSarcoglycansSgcd protein, mousefibrosismuscle regenerationmuscular dystrophy

Identifiers

PMID30216109
PMCPMC6338641
OpenAlexW2891865027

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.