Evidence map›Paper›PMID 28781131›Full record

ReviewEBioMedicine2017

Muscle Weakness in Rheumatoid Arthritis: The Role of Ca

Takashi Yamada, Maarten M Steinz, Ellinor Kenne, Johanna T Lanner

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.0field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

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  19. Skeletal muscle redox signaling in rheumatoid arthritis.Clinical science (London, England : 1979) · 2020
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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

4 authors at 2 institutions in 2 countries.

Takashi YamadaGraduate School of Health Sciences, Sapporo Medical University, Sapporo, Japan.
Maarten M SteinzDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Ellinor KenneDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Johanna T LannerDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden. Electronic address: Johanna.Lanner@ki.se.
Karolinska Institutet · SESapporo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to the primary symptoms arising from inflammatory processes in the joints, muscle weakness is commonly reported by patients with rheumatoid arthritis (RA). Muscle weakness not only reduces the quality of life for the affected patients, but also dramatically increases the burden on society since patients' work ability decreases. A 25-70% reduction in muscular strength has been observed in pateints with RA when compared with age-matched healthy controls. The reduction in muscle strength is often larger than what could be explained by the reduction in muscle size in patients with RA, which indicates that intracellular (intrinsic) muscle dysfunction plays an important role in the underlying mechanism of muscle weakness associated with RA. In this review, we highlight the present understanding of RA-associated muscle weakness with special focus on how enhanced Ca

Indexed as

Signal TransductionAnimalsAntioxidantsArthritis, RheumatoidCalciumCytokinesDisease ProgressionExcitation Contraction CouplingFemaleFree RadicalsHumansInflammation MediatorsMaleMuscle, SkeletalMuscle WeaknessMyofibrilsAntioxidantsCalciumCytokinesFree RadicalsInflammation MediatorsReactive Nitrogen SpeciesReactive Oxygen SpeciesRyanodine Receptor Calcium Release ChannelCa(2+)Muscle weaknessNitrosative stressPeroxynitriteRheumatoid arthritisRyanodine receptor

Identifiers

PMID28781131
PMCPMC5605300
OpenAlexW2739072801

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.