Evidence map›Paper›PMID 33920198›Full record

ArticleInternational journal of molecular sciences2021

Chronic Ouabain Prevents Na,K-ATPase Dysfunction and Targets AMPK and IL-6 in Disused Rat Soleus Muscle.

Violetta V Kravtsova, Inna I Paramonova, Natalia A Vilchinskaya, Maria V Tishkova, Vladimir V Matchkov, Boris S Shenkman, Igor I Krivoi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

7 authors at 3 institutions in 2 countries.

Violetta V KravtsovaDepartment of General Physiology, St. Petersburg State University, 199034 St. Petersburg, Russia.
Inna I ParamonovaMyology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.
Natalia A VilchinskayaMyology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.
Maria V TishkovaDepartment of General Physiology, St. Petersburg State University, 199034 St. Petersburg, Russia.
Vladimir V MatchkovDepartment of Biomedicine, MEMBRANES, Health, University of Aarhus, C 8000 Aarhus, Denmark.ORCID 0000-0002-3303-1095
Boris S ShenkmanMyology Laboratory, Institute of Biomedical Problems RAS, 123007 Moscow, Russia.
Igor I KrivoiDepartment of General Physiology, St. Petersburg State University, 199034 St. Petersburg, Russia.ORCID 0000-0002-2690-9226
Institute of Biomedical Problems · RUSt Petersburg University · RUAarhus University · DK

Funding

Novo Nordisk Fonden 18OC0052021Novo Nordisk Fonden 19OC0056371Russian Foundation for Basic Research 19-015-00319Russian Science Foundation 18-15-00043
6 · The paper itself

Abstract

Sustained sarcolemma depolarization due to loss of the Na,K-ATPase function is characteristic for skeletal muscle motor dysfunction. Ouabain, a specific ligand of the Na,K-ATPase, has a circulating endogenous analogue. We hypothesized that the Na,K-ATPase targeted by the elevated level of circulating ouabain modulates skeletal muscle electrogenesis and prevents its disuse-induced disturbances. Isolated soleus muscles from rats intraperitoneally injected with ouabain alone or subsequently exposed to muscle disuse by 6-h hindlimb suspension (HS) were studied. Conventional electrophysiology, Western blotting, and confocal microscopy with cytochemistry were used. Acutely applied 10 nM ouabain hyperpolarized the membrane. However, a single injection of ouabain (1 µg/kg) prior HS was unable to prevent the HS-induced membrane depolarization. Chronic administration of ouabain for four days did not change the α1 and α2 Na,K-ATPase protein content, however it partially prevented the HS-induced loss of the Na,K-ATPase electrogenic activity and sarcolemma depolarization. These changes were associated with increased phosphorylation levels of AMP-activated protein kinase (AMPK), its substrate acetyl-CoA carboxylase and p70 protein, accompanied with increased mRNA expression of interleikin-6 (IL-6) and IL-6 receptor. Considering the role of AMPK in regulation of the Na,K-ATPase, we suggest an IL-6/AMPK contribution to prevent the effects of chronic ouabain under skeletal muscle disuse.

Indexed as

Acetyl-CoA CarboxylaseAMP-Activated Protein Kinase KinasesAnimalsHindlimbHindlimb SuspensionHumansInterleukin-6Interleukin-6 InhibitorsMuscle, SkeletalMuscular Disorders, AtrophicOrgan Culture TechniquesOuabainProtein KinasesRatsRats, WistarSodium-Potassium-Exchanging ATPaseAcetyl-CoA CarboxylaseAMP-Activated Protein Kinase KinasesInterleukin-6Interleukin-6 InhibitorsOuabainProtein KinasesSodium-Potassium-Exchanging ATPaseAMP-activated protein kinasehindlimb suspensionNa,K-ATPase isozymesouabainresting membrane potentialskeletal muscle

Identifiers

PMID33920198
PMCPMC8069997
OpenAlexW3156941520

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.