Evidence map›Paper›PMID 27625424›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Role of dystroglycan in limiting contraction-induced injury to the sarcomeric cytoskeleton of mature skeletal muscle.

Erik P Rader, Rolf Turk, Tobias Willer, Daniel Beltrán, Kei-Ichiro Inamori, Taylor A Peterson, Jeffrey Engle, Sally Prouty, Kiichiro Matsumura, Fumiaki Saito and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

39 citing papers in PubMed, 51 citations in OpenAlex.

  1. Cytoplasmic region of beta-dystroglycan is essential for postsynaptic maturation and neuromuscular function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Improvement of Spontaneous Locomotor Activity in a Murine Model of Duchenne Muscular Dystrophy by N-Acetylglucosamine Alone and in Combination With Prednisolone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Plasma Proteomic Kinetics in Response to Acute Exercise.Molecular & cellular proteomics : MCP · 2023
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Lipotoxicity-related sarcopenia: a review.Journal of medicine and life · 2022
    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

12 authors at 4 institutions in 2 countries.

Erik P RaderHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Rolf TurkHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Tobias WillerHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Daniel BeltránHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Kei-Ichiro InamoriHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242; Division of Glycopathology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Miyagi 981-8558, Japan;
Taylor A PetersonHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Jeffrey EngleHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Sally ProutyHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Kiichiro MatsumuraDepartment of Neurology, Teikyo University School of Medicine, Itabashi-ku, Tokoyo 173-8605, Japan.
Fumiaki SaitoDepartment of Neurology, Teikyo University School of Medicine, Itabashi-ku, Tokoyo 173-8605, Japan.
Mary E AndersonHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242;
Kevin P CampbellHoward Hughes Medical Institute, The University of Iowa, Iowa City, IA 52242; Department of Molecular Physiology and Biophysics, The University of Iowa, Iowa City, IA 52242; Department of Neurology, The University of Iowa, Iowa City, IA 52242; Department of Internal Medicine, The University of Iowa, Iowa City, IA 52242; kevin-campbell@uiowa.edu.
University of Iowa · USHoward Hughes Medical Institute · USTeikyo University · JPTohoku Medical and Pharmaceutical University · JP

Funding

Therapeutic Potential of ESC-Derived Myogenic PrecursorsU54NS053672 · NINDS · UNIVERSITY OF IOWA · PI CAMPBELL, KEVIN P. · 2005 to 2019
$22.0M
INTERDISCIPLINARY CARDIOVASCULAR RESEARCH FELLOWSHIPT32HL007121 · NHLBI · UNIVERSITY OF IOWA · PI LONDON, BARRY · 1985 to 2020
$15.1M
NHLBI NIH HHS T32 HL007121NINDS NIH HHS U54 NS053672
6 · The paper itself

Abstract

Dystroglycan (DG) is a highly expressed extracellular matrix receptor that is linked to the cytoskeleton in skeletal muscle. DG is critical for the function of skeletal muscle, and muscle with primary defects in the expression and/or function of DG throughout development has many pathological features and a severe muscular dystrophy phenotype. In addition, reduction in DG at the sarcolemma is a common feature in muscle biopsies from patients with various types of muscular dystrophy. However, the consequence of disrupting DG in mature muscle is not known. Here, we investigated muscles of transgenic mice several months after genetic knockdown of DG at maturity. In our study, an increase in susceptibility to contraction-induced injury was the first pathological feature observed after the levels of DG at the sarcolemma were reduced. The contraction-induced injury was not accompanied by increased necrosis, excitation-contraction uncoupling, or fragility of the sarcolemma. Rather, disruption of the sarcomeric cytoskeleton was evident as reduced passive tension and decreased titin immunostaining. These results reveal a role for DG in maintaining the stability of the sarcomeric cytoskeleton during contraction and provide mechanistic insight into the cause of the reduction in strength that occurs in muscular dystrophy after lengthening contractions.

Indexed as

Muscle ContractionAnimalsConnectinCytoskeletonDystroglycansExcitation Contraction CouplingFemaleIsometric ContractionMaleMice, KnockoutMuscle, SkeletalNecrosisOrgan SizeRNA, MessengerSarcolemmaSarcomeresConnectinDystroglycansRNA, MessengerTamoxifendystroglycaneccentric contractionmuscular dystrophyskeletal muscletitin

Identifiers

PMID27625424
PMCPMC5047148
OpenAlexW2520132568

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.