Evidence map›Paper›PMID 26690705›Full record

ArticleThe Journal of clinical investigation2016

The AMPK-related kinase SNARK regulates muscle mass and myocyte survival.

Sarah J Lessard, Donato A Rivas, Kawai So, Ho-Jin Koh, André Lima Queiroz, Michael F Hirshman, Roger A Fielding, Laurie J Goodyear

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2016. 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
1.7field-weighted citation impact, top 16% 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, 36 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Supplementing Diets withAnimals : an open access journal from MDPI · 2022
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. AMPK in skeletal muscle function and metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Review
  15. Article
  16. Article
  17. Article
  18. Regulation of exercise-stimulated glucose uptake in skeletal muscle.Annals of pediatric endocrinology & metabolism · 2016
    Review
  19. 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

8 authors at 4 institutions in 1 country.

Sarah J Lessard
Donato A Rivas
Kawai So
Ho-Jin Koh
André Lima Queiroz
Michael F Hirshman
Roger A Fielding
Laurie J Goodyear
Joslin Diabetes Center · USTufts University · USBrigham and Women's Hospital · USHarvard University · US

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI JEAN E. SCHAFFER · 1986 to 2026
$50.5M
ROLE OF DIETARY CONSTITUENTS ON GENE EXPRESSION IN INTESTINAL EPITHELIUMP30DK040561 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI CHRISTOPHER P DUGGAN · 1994 to 2026
$31.6M
EXERCISE AND SKELETAL MUSCLE SIGNALING MECHANISMSR01AR042238 · NIAMS · JOSLIN DIABETES CENTER · PI GOODYEAR, LAURIE J · 1997 to 2013
$4.2M
Regultion of Serine/Threonine Kinases in Skeletal MuscleR01DK068626 · NIDDK · JOSLIN DIABETES CENTER · PI GOODYEAR, LAURIE J · 2004 to 2012
$3.5M
EXERCISE AND SKELETAL MUSCLE SIGNALING MECHANISMSR29AR042238 · NIAMS · JOSLIN DIABETES CENTER · PI GOODYEAR, LAURIE J · 1993 to 1996
–
NIAMS NIH HHS AR42238NIAMS NIH HHS R01 AR042238NIDDK NIH HHS DK068626NIDDK NIH HHS P30 DK036836NIDDK NIH HHS P30 DK040561NIDDK NIH HHS P30DK040561NIDDK NIH HHS P30 DK36836NIDDK NIH HHS R01 DK068626
6 · The paper itself

Abstract

The maintenance of skeletal muscle mass is critical for sustaining health; however, the mechanisms responsible for muscle loss with aging and chronic diseases, such as diabetes and obesity, are poorly understood. We found that expression of a member of the AMPK-related kinase family, the SNF1-AMPK-related kinase (SNARK, also known as NUAK2), increased with muscle cell differentiation. SNARK expression increased in skeletal muscles from young mice exposed to metabolic stress and in muscles from healthy older human subjects. The regulation of SNARK expression in muscle with differentiation and physiological stress suggests that SNARK may function in the maintenance of muscle mass. Consistent with this hypothesis, decreased endogenous SNARK expression (using siRNA) in cultured muscle cells resulted in increased apoptosis and decreased cell survival under conditions of metabolic stress. Likewise, muscle-specific transgenic animals expressing a SNARK dominant-negative inactive mutant (SDN) had increased myonuclear apoptosis and activation of apoptotic mediators in muscle. Moreover, animals expressing SDN had severe, age-accelerated muscle atrophy and increased adiposity, consistent with sarcopenic obesity. Reduced SNARK activity, in vivo and in vitro, caused downregulation of the Rho kinase signaling pathway, a key mediator of cell survival. These findings reveal a critical role for SNARK in myocyte survival and the maintenance of muscle mass with age.

Indexed as

ApoptosisGene Expression Regulation, EnzymologicSignal TransductionAgingAnimalsHumansMiceMice, TransgenicMuscle Fibers, SkeletalMuscular AtrophyOrgan SizeProtein Serine-Threonine Kinasesrho-Associated KinasesProtein Serine-Threonine Kinasesrho-Associated KinasesSNARK protein, mouse

Identifiers

PMID26690705
PMCPMC4731174
OpenAlexW2214992867

What OpenQuestion holds

Textmetadata
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.