Evidence map›Paper›PMID 24146652›Full record

ReviewFrontiers in physiology2013

Alterations of cAMP-dependent signaling in dystrophic skeletal muscle.

Rüdiger Rudolf, Muzamil M Khan, Danilo Lustrino, Siegfried Labeit, Isis C Kettelhut, Luiz C C Navegantes

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Targeting the sarcomere to correct muscle function.Nature reviews. Drug discovery · 2015
    Review
  17. Myopathic changes in murine skeletal muscle lacking synemin.American journal of physiology. Cell physiology · 2015
    Article
  18. Article
  19. Autonomic regulation in muscular dystrophy.Frontiers in physiology · 2014
    Article
  20. 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

6 authors at 4 institutions in 2 countries.

Rüdiger RudolfInstitute of Molecular and Cell Biology, University of Applied Sciences Mannheim , Mannheim, Germany ; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology , Eggenstein-Leopoldshafen, Germany.
Muzamil M Khan
Danilo Lustrino
Siegfried Labeit
Isis C Kettelhut
Luiz C C Navegantes
Clinics Hospital of Ribeirão Preto · BRKarlsruhe Institute of Technology · DEUniversidade de São Paulo · BRUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autonomic regulation processes in striated muscles are largely mediated by cAMP/PKA-signaling. In order to achieve specificity of signaling its spatial-temporal compartmentation plays a critical role. We discuss here how specificity of cAMP/PKA-signaling can be achieved in skeletal muscle by spatio-temporal compartmentation. While a microdomain containing PKA type I in the region of the neuromuscular junction (NMJ) is important for postsynaptic, activity-dependent stabilization of the nicotinic acetylcholine receptor (AChR), PKA type I and II microdomains in the sarcomeric part of skeletal muscle are likely to play different roles, including the regulation of muscle homeostasis. These microdomains are due to specific A-kinase anchoring proteins, like rapsyn and myospryn. Importantly, recent evidence indicates that compartmentation of the cAMP/PKA-dependent signaling pathway and pharmacological activation of cAMP production are aberrant in different skeletal muscles disorders. Thus, we discuss here their potential as targets for palliative treatment of certain forms of dystrophy and myasthenia. Under physiological conditions, the neuropeptide, α-calcitonin-related peptide, as well as catecholamines are the most-mentioned natural triggers for activating cAMP/PKA signaling in skeletal muscle. While the precise domains and functions of these first messengers are still under investigation, agonists of β2-adrenoceptors clearly exhibit anabolic activity under normal conditions and reduce protein degradation during atrophic periods. Past and recent studies suggest direct sympathetic innervation of skeletal muscle fibers. In summary, the organization and roles of cAMP-dependent signaling in skeletal muscle are increasingly understood, revealing crucial functions in processes like nerve-muscle interaction and muscle trophicity.

Indexed as

adrenoceptorsAKAPdystrophyendplatemetabolismneuromuscular junctionPKAskeletal muscle

Identifiers

PMID24146652
PMCPMC3797997
OpenAlexW2023052494

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.