Evidence map›Paper›PMID 32972442›Full record

ArticleJournal of translational medicine2020

A SWATH-MS analysis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome peripheral blood mononuclear cell proteomes reveals mitochondrial dysfunction.

Eiren Sweetman, Torsten Kleffmann, Christina Edgar, Michel de Lange, Rosamund Vallings, Warren Tate

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 3 pooled it
7.9field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 3 syntheses or guidelines pooled it, 83 citations in OpenAlex.

  1. Pooled it
  2. Recent research in myalgic encephalomyelitis/chronic fatigue syndrome: an evidence map.Health technology assessment (Winchester, England) · 2025
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  20. Measuring Biomarkers of Oxidative Stress in ME/CFS Patients.Methods in molecular biology (Clifton, N.J.) · 2025
    Article

2 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Eiren SweetmanDepartment of Biochemistry, University of Otago, Dunedin, 9016, New Zealand.ORCID 0000-0002-1687-2714
Torsten KleffmannDepartment of Biochemistry, University of Otago, Dunedin, 9016, New Zealand.
Christina EdgarDepartment of Biochemistry, University of Otago, Dunedin, 9016, New Zealand.
Michel de LangeCentre for Biostatistics, University of Otago, Dunedin, 9016, New Zealand.
Rosamund VallingsHowick Health and Medical Centre, Auckland, 2014, New Zealand.
Warren TateDepartment of Biochemistry, University of Otago, Dunedin, 9016, New Zealand. warren.tate@otago.ac.nz.
University of Otago · NZ

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a serious and complex physical illness that affects all body systems with a multiplicity of symptoms, but key hallmarks of the disease are pervasive fatigue and 'post-exertional malaise', exacerbation after physical and/or mental activity of the intrinsic fatigue and other symptoms that can be highly debilitating and last from days to months. Although the disease can vary widely between individuals, common symptoms also include pain, cognitive deficits, sleep dysfunction, as well as immune, neurological and autonomic symptoms. Typically, it is a very isolating illness socially, carrying a stigma because of the lack of understanding of the cause and pathophysiology.

methodsTo gain insight into the pathophysiology of ME/CFS, we examined the proteomes of peripheral blood mononuclear cells (PBMCs) by SWATH-MS analysis in a small well-characterised group of patients and matched controls. A principal component analysis (PCA) was used to stratify groups based on protein abundance patterns, which clearly segregated the majority of the ME/CFS patients (9/11) from the controls. This majority subgroup of ME/CFS patients was then further compared to the control group.

resultsA total of 60 proteins in the ME/CFS patients were differentially expressed (P < 0.01, Log

conclusionsThe results from this study support a model of deficient ATP production in ME/CFS, compensated for by upregulation of immediate pathways upstream of Complex V that would suggest an elevation of oxidative stress. This study and others have found evidence of a distinct pathology in ME/CFS that holds promise for developing diagnostic biomarkers.

Indexed as

Fatigue Syndrome, ChronicDNA MethylationHumansLeukocytes, MononuclearMitochondriaProteomeProteomeChronic fatigue syndromeDiagnostic biomarkerInflammation and immunityMetabolismMitochondriaMyalgic encephalomyelitisOxidative phosphorylationOxidative stressReactive oxygen species

Identifiers

PMID32972442
PMCPMC7512220
OpenAlexW3089319547

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.