Evidence map›Paper›PMID 33825942›Full record

ReviewCellular and molecular life sciences : CMLS2021

Therapeutic aspects of cell signaling and communication in Duchenne muscular dystrophy.

Alicja Starosta, Patryk Konieczny

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

23 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Caveolin and NOS in the Development of Muscular Dystrophy.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Article
  10. Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Cells · 2021
    Review
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

2 authors at 1 institution in 1 country.

Alicja StarostaFaculty of Biology, Institute of Human Biology and Evolution, Adam Mickiewicz University, ul. Uniwersytetu Poznańskiego 6, 61-614, Poznań, Poland.
Patryk KoniecznyFaculty of Biology, Institute of Human Biology and Evolution, Adam Mickiewicz University, ul. Uniwersytetu Poznańskiego 6, 61-614, Poznań, Poland. patryk.konieczny@amu.edu.pl.ORCID http://orcid.org/0000-0002-9609-8254
Adam Mickiewicz University in Poznań · PL

Funding

Narodowe Centrum Nauki 2018/30/E/NZ5/00065
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a devastating chromosome X-linked disease that manifests predominantly in progressive skeletal muscle wasting and dysfunctions in the heart and diaphragm. Approximately 1/5000 boys and 1/50,000,000 girls suffer from DMD, and to date, the disease is incurable and leads to premature death. This phenotypic severity is due to mutations in the DMD gene, which result in the absence of functional dystrophin protein. Initially, dystrophin was thought to be a force transducer; however, it is now considered an essential component of the dystrophin-associated protein complex (DAPC), viewed as a multicomponent mechanical scaffold and a signal transduction hub. Modulating signal pathway activation or gene expression through epigenetic modifications has emerged at the forefront of therapeutic approaches as either an adjunct or stand-alone strategy. In this review, we propose a broader perspective by considering DMD to be a disease that affects myofibers and muscle stem (satellite) cells, as well as a disorder in which abrogated communication between different cell types occurs. We believe that by taking this systemic view, we can achieve safe and holistic treatments that can restore correct signal transmission and gene expression in diseased DMD tissues.

Indexed as

Cell CommunicationSignal TransductionAnimalsBone and BonesDystrophinHumansMicrovesselsMuscle, SkeletalMuscular Dystrophy, DuchenneNeuronsDystrophinDMDDuchenne muscular dystrophySignaling pathwaysStriated muscles

Identifiers

PMID33825942
PMCPMC8233280
OpenAlexW3146846567

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.