ArticleRMD open2025
Mitochondrial dysfunction and fatigue in Sjögren's disease.
Article in RMD open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Mitochondrial Dysfunction in Circulating Blood Cells and Biological Aging: A Review of Mechanisms and Evidence.Biomolecules · 2026Review
- Mitophagy and Immune Infiltration in Primary Sjögren's Disease: Insights from Bioinformatics Analysis.International journal of molecular sciences · 2026Article
- The NLRP3 inflammasome as a key pathway in the affective and chronic fatigue symptoms of Long COVID.Journal of translational medicine · 2026Article
- Mediterranean diet and symptom severity in Sjogren's syndrome.Frontiers in medicine · 2026Article
- Immune remodeling and metabolic reprogramming in chronic fatigue: insights into GPCR signaling and epigenetic regulation.Frontiers in immunology · 2026Review
- Mitophagy as a therapeutic target for exercise-induced fatigue: modulation by natural compounds and mechanistic insights.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
objectiveSjögren's disease (SjD) is a chronic exocrine disorder typified by inflammation and dryness, but also profound fatigue, suggesting a pathological basis in cellular bioenergetics. In healthy states, dysfunctional mitochondria are recycled by mitophagic processes; when impaired, poorly functioning mitochondria persist and produce inflammatory reactive oxygen species. Employing a case-control study, we tested our hypothesis that mitochondrial dysregulation in T cells is associated with fatigue in SjD.
methodsWe isolated pan T cells from peripheral blood mononuclear cells of 13 SjD and 4 non-Sjögren's sicca (NSS) subjects, who completed several fatigue questionnaires, along with 8 healthy subjects. Using Seahorse, we analysed T cells for mitochondrial oxygen consumption rate (OCR) and extracellular acidification rate, which we assessed for correlation with fatigue measures. Using public microarray data available for 190 SjD and 32 healthy subjects, we identified a mitophagic transcriptional signature that stratified SjD patients into 5 discrete clusters. Comparisons between the SjD subjects in these clusters to healthy individuals identified differentially expressed transcripts, which we subjected to bioinformatic interrogation.
resultsBasal OCR, ATP-linked respiration, maximal respiration and reserve capacity were significantly lower in SjD and NSS subjects compared with healthy individuals, with no differences in non-mitochondrial respiration, basal glycolysis or glycolytic reserve. Scores related to a sleep questionnaire and Bowman's Profile of Fatigue and Discomfort showed correlation with altered OCR in SjD. Subgroup differential expression analysis revealed dynamic transcriptional activity between mitophagy subgroups, expanding the number of differentially expressed transcripts tenfold.
conclusionsMitochondrial dysfunction and fatigue are significant problems in SjD warranting further investigation.
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Registered trials
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 Socratic graph.