Evidence map›Paper›PMID 25104934›Full record

ReviewFrontiers in aging neuroscience2014

Skeletal muscle homeostasis in duchenne muscular dystrophy: modulating autophagy as a promising therapeutic strategy.

Clara De Palma, Cristiana Perrotta, Paolo Pellegrino, Emilio Clementi, Davide Cervia

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

36 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
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  8. Cyclo His-Pro Attenuates Muscle Degeneration in Murine Myopathy Models.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  9. Review
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  15. Review
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  17. Review
  18. Duchenne muscular dystrophy.Nature reviews. Disease primers · 2021
    Review
  19. 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

5 authors at 3 institutions in 1 country.

Clara De PalmaUnit of Clinical Pharmacology, Department of Biomedical and Clinical Sciences "L. Sacco", National Research Council-Institute of Neuroscience, University Hospital "L. Sacco", University of Milan , Milan , Italy.
Cristiana PerrottaUnit of Clinical Pharmacology, Department of Biomedical and Clinical Sciences "L. Sacco", National Research Council-Institute of Neuroscience, University Hospital "L. Sacco", University of Milan , Milan , Italy.
Paolo PellegrinoUnit of Clinical Pharmacology, Department of Biomedical and Clinical Sciences "L. Sacco", National Research Council-Institute of Neuroscience, University Hospital "L. Sacco", University of Milan , Milan , Italy.
Emilio ClementiUnit of Clinical Pharmacology, Department of Biomedical and Clinical Sciences "L. Sacco", National Research Council-Institute of Neuroscience, University Hospital "L. Sacco", University of Milan , Milan , Italy ; Scientific Institute IRCCS Eugenio Medea , Bosisio Parini , Italy.
Davide CerviaUnit of Clinical Pharmacology, Department of Biomedical and Clinical Sciences "L. Sacco", National Research Council-Institute of Neuroscience, University Hospital "L. Sacco", University of Milan , Milan , Italy ; Department for Innovation in Biological, Agro-Food and Forest Systems, University of Tuscia , Viterbo , Italy.
National Research Council · ITUniversity of Milan · ITUniversità degli Studi della Tuscia · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscular dystrophies are a group of genetic and heterogeneous neuromuscular disorders characterized by the primary wasting of skeletal muscle. In Duchenne muscular dystrophy (DMD), the most severe form of these diseases, the mutations in the dystrophin gene lead to muscle weakness and wasting, exhaustion of muscular regenerative capacity, and chronic local inflammation leading to substitution of myofibers by connective and adipose tissue. DMD patients suffer from continuous and progressive skeletal muscle damage followed by complete paralysis and death, usually by respiratory and/or cardiac failure. No cure is yet available, but several therapeutic approaches aiming at reversing the ongoing degeneration have been investigated in preclinical and clinical settings. Autophagy is an important proteolytic system of the cell and has a crucial role in the removal of proteins, aggregates, and organelles. Autophagy is constantly active in skeletal muscle and its role in tissue homeostasis is complex: at high levels, it can be detrimental and contribute to muscle wasting; at low levels, it can cause weakness and muscle degeneration, due to the unchecked accumulation of damaged proteins and organelles. The causal relationship between DMD pathogenesis and dysfunctional autophagy has been recently investigated. At molecular level, the Akt axis is one of the key dysregulated pathways, although the molecular events are not completely understood. The aim of this review is to describe and discuss the clinical relevance of the recent advances dissecting autophagy and its signaling pathway in DMD. The picture might pave the way for the development of interventions that are able to boost muscle growth and/or prevent muscle wasting.

Indexed as

Akt–mTOR axisautophagyDuchenne muscular dystrophymdx micemuscle wastingskeletal muscletherapeutic target

Identifiers

PMID25104934
PMCPMC4109521
OpenAlexW2107867413

What OpenQuestion 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 OpenQuestion graph.