Evidence map›Paper›PMID 20817957›Full record

ArticleAging2010

Muscle-specific inositide phosphatase (MIP/MTMR14) is reduced with age and its loss accelerates skeletal muscle aging process by altering calcium homeostasis.

Sandra Romero-Suarez, Jinhua Shen, Leticia Brotto, Todd Hall, Chenglin Mo, Héctor H Valdivia, Jon Andresen, Michael Wacker, Thomas M Nosek, Cheng-Kui Qu and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Mouse models of sarcopenia: classification and evaluation.Journal of cachexia, sarcopenia and muscle · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Longevity, aging and rapamycin.Cellular and molecular life sciences : CMLS · 2014
    Review
  18. Genetically enhancing mitochondrial antioxidant activity improves muscle function in aging.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  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

11 authors at 3 institutions in 1 country.

Sandra Romero-SuarezMuscle Biology Research Group-MUBIG, Schools of Nursing, University of Missouri-Kansas City, Kansas City, MO 64108, USA.
Jinhua Shen
Leticia Brotto
Todd Hall
Chenglin Mo
Héctor H Valdivia
Jon Andresen
Michael Wacker
Thomas M Nosek
Cheng-Kui Qu
Marco Brotto
University of Missouri–Kansas City · USCase Western Reserve University · USUniversity of Wisconsin–Madison · US

Funding

Ryanodine Receptors, Calcium-dependent Arrhythmias & HCMR01HL055438 · NHLBI · UNIVERSITY OF WISCONSIN-MADISON · PI VALDIVIA, HECTOR H · 1996 to 2023
$8.0M
Tyrosine Phosphatases and Hematopoietic Cell RegulationR01HL068212 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI QU, CHENG-KUI · 2002 to 2012
$3.2M
Muscle-Bone Endocrine AxisRC2AR058962 · NIAMS · UNIVERSITY OF MISSOURI KANSAS CITY · PI BONEWALD, LYNDA F, BROTTO, MARCO · 2009 to 2010
$1.1M
SHP-2 Inhibitors as Potential Therapeutic Agents for JMML and Noonan SyndromeR21HL082670 · NHLBI · CASE WESTERN RESERVE UNIVERSITY · PI QU, CHENG-KUI · 2007 to 2008
$431k
NHLBI NIH HHS HL068212NHLBI NIH HHS HL082670NHLBI NIH HHS HL55438NHLBI NIH HHS R01 HL055438NHLBI NIH HHS R01 HL068212NHLBI NIH HHS R21 HL082670NIAMS NIH HHS 1RC2AR058962-01NIAMS NIH HHS RC2 AR058962
6 · The paper itself

Abstract

We have recently reported that a novel muscle-specific inositide phosphatase (MIP/MTMR14) plays a critical role in [Ca2+]i homeostasis through dephosphorylation of sn-1-stearoyl-2-arachidonoyl phosphatidylinositol (3,5) bisphosphate (PI(3,5)P2). Loss of function mutations in MIP have been identified in human centronuclear myopathy. We developed a MIP knockout (MIPKO) animal model and found that MIPKO mice were more susceptible to exercise-induced muscle damage, a trademark of muscle functional changes in older subjects. We used wild-type (Wt) mice and MIPKO mice to elucidate the roles of MIP in muscle function during aging. We found MIP mRNA expression, MIP protein levels, and MIP phosphatase activity significantly decreased in old Wt mice. The mature MIPKO mice displayed phenotypes that closely resembled those seen in old Wt mice: i) decreased walking speed, ii) decreased treadmill activity, iii) decreased contractile force, and iv) decreased power generation, classical features of sarcopenia in rodents and humans. Defective Ca2+ homeostasis is also present in mature MIPKO and old Wt mice, suggesting a putative role of MIP in the decline of muscle function during aging. Our studies offer a new avenue for the investigation of MIP roles in skeletal muscle function and as a potential therapeutic target to treat aging sarcopenia.

Indexed as

SarcopeniaAgingAnimalsCalciumCellular SenescenceDisease Models, AnimalGene Expression RegulationHumansMiceMice, KnockoutMuscle, SkeletalMutationMyopathies, Structural, CongenitalPhenotypePhosphatidylinositolsPhosphoric Monoester Hydrolases1-stearoyl-2-arachidonoyl phosphatidylinositolCalciumMTMR14 protein, humanMTMR14 protein, mousePhosphatidylinositolsPhosphoric Monoester Hydrolases

Identifiers

PMID20817957
PMCPMC2954041
OpenAlexW2149356606

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.