ArticleMolecular medicine (Cambridge, Mass.)2018
Loss of Transient Receptor Potential Melastatin 3 ion channel function in natural killer cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients.
Article in Molecular medicine (Cambridge, Mass.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 4 of them syntheses that pooled it.
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Who cites it
34 citing papers in PubMed, 4 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Biomarkers for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): a systematic review.BMC medicine · 2023Pooled it
- Neuroimaging characteristics of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): a systematic review.Journal of translational medicine · 2020Pooled it
- A systematic review of mitochondrial abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome/systemic exertion intolerance disease.Journal of translational medicine · 2020Pooled it
- A systematic review of natural killer cells profile and cytotoxic function in myalgic encephalomyelitis/chronic fatigue syndrome.Systematic reviews · 2019Pooled it
- Naltrexone Restores Impaired Transient Receptor Potential Melastatin 3 Ion Channel Function in Natural Killer Cells From Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients.Frontiers in immunology · 2019Trial
- Deficient TRPM3-linked mitochondrial CaBMC immunology · 2026Article
- Imbalance of Excitatory and Inhibitory Neurotransmitter Systems in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2026Review
- The search for a blood-based biomarker for Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome (ME/CFS): from biochemistry to electrophysiology.Journal of translational medicine · 2025Review
- The potential causes of myasthenia and fasciculations in severely ill ME/CFS patients: the role of disturbed electrophysiology.Frontiers in physiology · 2025Article
- Analysis of Transient Receptor Potential Ion Channels in ME/CFS.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Absence of BOLD adaptation in chronic fatigue syndrome revealed by task functional MRI.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Observational
- Large-scale investigation confirms TRPM3 ion channel dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Frontiers in medicine · 2025Article
- Low-Dose naltrexone restored TRPM3 ion channel function in natural killer cells from long COVID patients.Frontiers in molecular biosciences · 2025Article
- Identifying microRNAs Possibly Implicated in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome and Fibromyalgia: A Review.International journal of molecular sciences · 2024Review
- Potential pathophysiological role of the ion channel TRPM3 in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and the therapeutic effect of low-dose naltrexone.Journal of translational medicine · 2024Review
- Novel characterization of endogenous transient receptor potential melastatin 3 ion channels from Gulf War Illness participants.PloS one · 2024Article
- Investigation into the restoration of TRPM3 ion channel activity in post-COVID-19 condition: a potential pharmacotherapeutic target.Frontiers in immunology · 2024Article
- Mitochondrial Dysfunction and Coenzyme Q10 Supplementation in Post-Viral Fatigue Syndrome: An Overview.International journal of molecular sciences · 2024Review
- Altered TRPM7-Dependent Calcium Influx in Natural Killer Cells of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome Patients.Biomolecules · 2023Article
- Altered brain connectivity in Long Covid during cognitive exertion: a pilot study.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChronic Fatigue Syndrome (CFS)/ Myalgic Encephalomyelitis (ME) is a debilitating disorder that is accompanied by reduced cytotoxic activity in natural killer (NK) cells. NK cells are an essential innate immune cell, responsible for recognising and inducing apoptosis of tumour and virus infected cells. Calcium is an essential component in mediating this cellular function. Transient Receptor Potential Melastatin 3 (TRPM3) cation channels have an important regulatory role in mediating calcium influx to help maintain cellular homeostasis. Several single nucleotide polymorphisms have been reported in TRPM3 genes from isolated peripheral blood mononuclear cells, NK and B cells in patients with CFS/ME and have been proposed to correlate with illness presentation. Moreover, a significant reduction in both TRPM3 surface expression and intracellular calcium mobilisation in NK cells has been found in CFS/ME patients compared with healthy controls. Despite the functional importance of TRPM3, little is known about the ion channel function in NK cells and the epiphenomenon of CFS/ME. The objective of the present study was to characterise the TRPM3 ion channel function in NK cells from CFS/ME patients in comparison with healthy controls using whole cell patch-clamp techniques.
methodsNK cells were isolated from 12 age- and sex-matched healthy controls and CFS patients. Whole cell electrophysiology recording has been used to assess TRPM3 ion channel activity after modulation with pregnenolone sulfate and ononetin.
resultsWe report a significant reduction in amplitude of TRPM3 current after pregnenolone sulfate stimulation in isolated NK cells from CFS/ME patients compared with healthy controls. In addition, we found pregnenolone sulfate-evoked ionic currents through TRPM3 channels were significantly modulated by ononetin in isolated NK cells from healthy controls compared with CFS/ME patients.
conclusionsTRPM3 activity is impaired in CFS/ME patients suggesting changes in intracellular Ca
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