ArticleJournal of translational medicine2019
A possible role for mitochondrial-derived peptides humanin and MOTS-c in patients with Q fever fatigue syndrome and chronic fatigue syndrome.
Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.
- Recent research in myalgic encephalomyelitis/chronic fatigue syndrome: an evidence map.Health technology assessment (Winchester, England) · 2025Pooled it
- No Signs of Neuroinflammation in Women With Chronic Fatigue Syndrome or Q Fever Fatigue Syndrome Using the TSPO Ligand [Neurology(R) neuroimmunology & neuroinflammation · 2022Trial
- Systematic Examination of Gene Expression and Proteomic Evidence Across Tissues Supports the Role of Mitochondrial Dysregulation in ME/CFS.International journal of molecular sciences · 2026Article
- Elevated Serum Nardilysin Is Inversely Associated with Cardiovascular Disease in Kidney Transplant Recipients.Kidney & blood pressure research · 2026Article
- Dysregulated Resolution of Inflammation After Respiratory Viral Infections: Molecular Pathways Linking Neuroinflammation to Post-Viral Neuropathic Pain-A Narrative Review.International journal of molecular sciences · 2025Review
- A Comprehensive Review of the Mechanisms of Human Q Fever: Pathogenesis and Pathophysiology.Pathogens (Basel, Switzerland) · 2025Review
- Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches.GeroScience · 2024Review
- Article
- Deep phenotyping of post-infectious myalgic encephalomyelitis/chronic fatigue syndrome.Nature communications · 2024Article
- MOTS-c Functionally Prevents Metabolic Disorders.Metabolites · 2023Review
- Article
- Bioinformatics and systems biology approach to identify the pathogenetic link of Long COVID and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Frontiers in immunology · 2022Article
- mapMECFS: a portal to enhance data discovery across biological disciplines and collaborative sites.Journal of translational medicine · 2021Article
- Severe Fatigue and Memory Impairment Are Associated with Lower Serum Level of Anti-SARS-CoV-2 Antibodies in Patients with Post-COVID Symptoms.Journal of clinical medicine · 2021Article
- Article
- Mitochondrial-encoded MOTS-c prevents pancreatic islet destruction in autoimmune diabetes.Cell reports · 2021Article
- Multi-omics examination of Q fever fatigue syndrome identifies similarities with chronic fatigue syndrome.Journal of translational medicine · 2020Article
- Role of the mitochondrial stress response in human cancer progression.Experimental biology and medicine (Maywood, N.J.) · 2020Review
- Mitonuclear genomics and aging.Human genetics · 2020Review
- MOTS-c: A Mitochondrial-Encoded Regulator of the Nucleus.BioEssays : news and reviews in molecular, cellular and developmental biology · 2019Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundQ fever fatigue syndrome (QFS) is a well-documented state of prolonged fatigue following around 20% of acute Q fever infections. It has been hypothesized that low grade inflammation plays a role in its aetiology. In this study, we aimed to identify transcriptome profiles that could aid to better understand the pathophysiology of QFS.
methodsRNA of monocytes was collected from QFS patients (n = 10), chronic fatigue syndrome patients (CFS, n = 10), Q fever seropositive controls (n = 10), and healthy controls (n = 10) who were age- (± 5 years) and sex-matched. Transcriptome analysis was performed using RNA sequencing.
resultsMitochondrial-derived peptide (MDP)-coding genes MT-RNR2 (humanin) and MT-RNR1 (MOTS-c) were differentially expressed when comparing QFS (- 4.8 log2-fold-change P = 2.19 × 10
conclusionsExpression of MDP-coding genes MT-RNR1 (MOTS-c) and MT-RNR2 (humanin) is decreased in CFS, QFS, and, to a lesser extent, in Q fever seropositive controls, resulting in a decreased production of humanin. These novel peptides might indeed be important in the pathophysiology of both QFS and CFS.
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Registered trials
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