Evidence map›Paper›PMID 18505477›Full record

ArticleAging cell2008

Compromised store-operated Ca2+ entry in aged skeletal muscle.

Xiaoli Zhao, Noah Weisleder, Angela Thornton, Yaa Oppong, Rachel Campbell, Jianjie Ma, Marco Brotto

Open access · bronzeAbstract read
In one paragraph

Article in Aging cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

65 citing papers in PubMed, 87 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025
    Review
  8. Article
  9. Article
  10. Store-operated CaPNAS nexus · 2023
    Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Altered CaMetabolites · 2021
    Review
  16. Improper Remodeling of Organelles Deputed to CaInternational journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. Review
  20. Review

5 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 1 country.

Xiaoli ZhaoDepartment of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA.
Noah Weisleder
Angela Thornton
Yaa Oppong
Rachel Campbell
Jianjie Ma
Marco Brotto
Rutgers, The State University of New Jersey · USUniversity of Missouri–Kansas City · US

Funding

Modulation of MG53 Function in Cardiac Membrane RepairR01HL069000 · NHLBI · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MA, JIANJIE · 2002 to 2016
$5.3M
TRIC, a Novel Modulator of Intracellular Ca HomeostasisR01AG028856 · NIA · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MA, JIANJIE · 2008 to 2012
$2.1M
NHLBI NIH HHS R01 HL069000NIA NIH HHS R01 AG028856
6 · The paper itself

Abstract

In aged skeletal muscle, changes to the composition and function of the contractile machinery cannot fully explain the observed decrease in the specific force produced by the contractile machinery that characterizes muscle weakness during aging. Since modification in extracellular Ca(2+) entry in aged nonexcitable and excitable cells has been recently identified, we evaluated the functional status of store-operated Ca(2+) entry (SOCE) in aged mouse skeletal muscle. Using Mn(2+) quenching of Fura-2 fluorescence and confocal-microscopic imaging of Ca(2+) movement from the transverse tubules, we determined that SOCE was severely compromised in muscle fibers isolated from aged mice (26-27 months) as compared with those from young (2-5 months) mice. While reduced SOCE in aged skeletal muscle does not appear to result from altered expression levels of STIM1 or reduced expression of mRNA for Orai, this reduction in SOCE is mirrored in fibers isolated from young mice null for mitsugumin-29, a synaptophysin-related protein that displays decreased expression in aged skeletal muscle. Our data suggest that decreased mitsugumin-29 expression and reduced SOCE may contribute to the diminished intracellular Ca(2+) homeostatic capacity generally associated with muscle aging.

Indexed as

Calcium SignalingAgingAnimalsCalciumCalcium ChannelsCell LineMaleManganeseMembrane GlycoproteinsMiceMice, Inbred C57BLMicroscopy, ConfocalMuscle Fibers, SkeletalMuscle ProteinsMuscle, SkeletalORAI1 ProteinCalciumCalcium ChannelsManganeseMembrane GlycoproteinsMg29 protein, mouseMuscle ProteinsORAI1 ProteinOrai1 protein, mouseStim1 protein, mouseStromal Interaction Molecule 1Synaptophysin

Identifiers

PMID18505477
PMCPMC2991086
OpenAlexW2077035040

What OpenQuestion holds

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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.