Evidence map›Paper›PMID 21364645›Full record

ArticleCell death & disease2010

c-Flip overexpression affects satellite cell proliferation and promotes skeletal muscle aging.

C Giampietri, S Petrungaro, P Coluccia, F Antonangeli, K Giannakakis, T Faraggiana, A Filippini, G Cossu, E Ziparo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Article
  3. Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Multifaceted Roles of GSK-3 in Cancer and Autophagy-Related Diseases.Oxidative medicine and cellular longevity · 2017
    Review
  10. FLIP the Switch: Regulation of Apoptosis and Necroptosis by cFLIP.International journal of molecular sciences · 2015
    Review
  11. Article
  12. Necroptosis: molecular signalling and translational implications.International journal of cell biology · 2014
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Cell death in disease: from 2010 onwards.Cell death & disease · 2011
    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

9 authors at 4 institutions in 1 country.

C GiampietriIstituto Pasteur-Fondazione Cenci Bolognetti, Department of Histology and Medical Embryology, Sapienza University of Rome, Rome, Italy.
S Petrungaro
P Coluccia
F Antonangeli
K Giannakakis
T Faraggiana
A Filippini
G Cossu
E Ziparo
Sapienza University of Rome · ITIstituto Pasteur · ITIstituto Dermopatico dell'Immacolata · ITUniversity of Milan · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study shows that forcing c-Flip overexpression in undifferentiated skeletal myogenic cells in vivo results in early aging muscle phenotype. In the transgenic mice, adult muscle histology, histochemistry and biochemistry show strong alterations: reduction of fibers size and muscle mass, mitochondrial abnormalities, increase in protein oxidation and apoptosis markers and reduced AKT/GSK3β phosphorylation. In the infant, higher levels of Pax-7, PCNA, P-ERK and active-caspase-3 were observed, indicating enhanced proliferation and concomitant apoptosis of myogenic precursors. Increased proliferation correlated with NF-κB activation, detected as p65 phosphorylation, and with high levels of embryonic myosin heavy chain. Reduced regenerative potential after muscle damage in the adult and impaired fiber growth associated with reduced NFATc2 activation in the infant were also observed, indicating that the satellite cell pool is prematurely compromised. Altogether, these data show a role for c-Flip in modulating skeletal muscle phenotype by affecting the proliferative potential of undifferentiated cells. This finding indicates a novel additional mechanism through which c-Flip might possibly control tissue remodeling.

Indexed as

AgingAnimalsApoptosisCASP8 and FADD-Like Apoptosis Regulating ProteinCell DifferentiationCell ProliferationFreezingGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaImmunohistochemistryMiceMice, TransgenicMuscle DevelopmentMuscle Fibers, SkeletalMuscle, SkeletalPromoter Regions, GeneticCASP8 and FADD-Like Apoptosis Regulating ProteinCflar protein, mouseGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, mouseProto-Oncogene Proteins c-akt

Identifiers

PMID21364645
PMCPMC3032302
OpenAlexW1996900286

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.