Evidence map›Paper›PMID 33669532›Full record

ArticleInternational journal of molecular sciences2021

Dysregulated Provision of Oxidisable Substrates to the Mitochondria in ME/CFS Lymphoblasts.

Daniel Missailidis, Oana Sanislav, Claire Y Allan, Paige K Smith, Sarah J Annesley, Paul R Fisher

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

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

  1. Recent research in myalgic encephalomyelitis/chronic fatigue syndrome: an evidence map.Health technology assessment (Winchester, England) · 2025
    Pooled it
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  14. Quantitative Proteomics on Immune Cells of ME/CFS Patients Using SWATH-MS.Methods in molecular biology (Clifton, N.J.) · 2025
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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

6 authors at 2 institutions in 1 country.

Daniel MissailidisDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC 3086, Australia.
Oana SanislavDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC 3086, Australia.
Claire Y AllanDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC 3086, Australia.
Paige K SmithMonash Health, Melbourne, VIC 3186, Australia.ORCID 0000-0002-0750-0468
Sarah J AnnesleyDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC 3086, Australia.ORCID 0000-0002-7604-3985
Paul R FisherDepartment of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Melbourne, VIC 3086, Australia.ORCID 0000-0003-1884-6306
La Trobe University · AUMonash Health · AU

Funding

Judith Jane Mason and Harold Stannett Williams Memorial Foundation MAS2016F063, MAS2018F00026
6 · The paper itself

Abstract

Although understanding of the biomedical basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is growing, the underlying pathological mechanisms remain uncertain. We recently reported a reduction in the proportion of basal oxygen consumption due to ATP synthesis by Complex V in ME/CFS patient-derived lymphoblast cell lines, suggesting mitochondrial respiratory inefficiency. This was accompanied by elevated respiratory capacity, elevated mammalian target of rapamycin complex 1 (mTORC1) signaling activity and elevated expression of enzymes involved in the TCA cycle, fatty acid β-oxidation and mitochondrial transport. These and other observations led us to hypothesise the dysregulation of pathways providing the mitochondria with oxidisable substrates. In our current study, we aimed to revisit this hypothesis by applying a combination of whole-cell transcriptomics, proteomics and energy stress signaling activity measures using subsets of up to 34 ME/CFS and 31 healthy control lymphoblast cell lines from our growing library. While levels of glycolytic enzymes were unchanged in accordance with our previous observations of unaltered glycolytic rates, the whole-cell proteomes of ME/CFS lymphoblasts contained elevated levels of enzymes involved in the TCA cycle (

Indexed as

AdultAgedFatigue Syndrome, ChronicFemaleGene Expression RegulationHumansLymphocytesMaleMetabolic Networks and PathwaysMiddle AgedMitochondriaOxidation-ReductionOxidative PhosphorylationProteasome Endopeptidase ComplexProtein SubunitsProteomeProteasome Endopeptidase ComplexProtein SubunitsProteomeRNA, Messengeramino acid catabolismbeta-oxidationglycolysisME/CFSmetabolismmitochondriaMyalgic EncephalomyelitisproteomicsTCA cycletranscriptomics

Identifiers

PMID33669532
PMCPMC7921983
OpenAlexW3131700307

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.