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Potential Implications of Mammalian Transient Receptor Potential Melastatin 7 in the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Review

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  • Stanley Du Preez

    (National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute, Griffith University, Gold Coast 4215, Australia
    Consortium Health International for Myalgic Encephalomyelitis, Menzies Health Institute Queensland, Griffith University, Gold Coast 4215, Australia
    School of Pharmacy and Medical Sciences, Griffith University, Gold Coast 4215, Australia
    School of Medicine and Dentistry, Griffith University, Gold Coast 4215, Australia)

  • Helene Cabanas

    (Consortium Health International for Myalgic Encephalomyelitis, Menzies Health Institute Queensland, Griffith University, Gold Coast 4215, Australia
    Institut de Recherche Saint Louis, Université de Paris, INSERM U944 and CNRS UMR 7212, Hôpital Saint Louis, APHP, 75010 Paris, France)

  • Donald Staines

    (National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute, Griffith University, Gold Coast 4215, Australia
    Consortium Health International for Myalgic Encephalomyelitis, Menzies Health Institute Queensland, Griffith University, Gold Coast 4215, Australia)

  • Sonya Marshall-Gradisnik

    (National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute, Griffith University, Gold Coast 4215, Australia
    Consortium Health International for Myalgic Encephalomyelitis, Menzies Health Institute Queensland, Griffith University, Gold Coast 4215, Australia)

Abstract

The transient receptor potential (TRP) superfamily of ion channels is involved in the molecular mechanisms that mediate neuroimmune interactions and activities. Recent advancements in neuroimmunology have identified a role for TRP cation channels in several neuroimmune disorders including amyotropic lateral sclerosis, multiple sclerosis, and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS is a debilitating disorder with an obscure aetiology, hence considerable examination of its pathobiology is warranted. Dysregulation of TRP melastatin (TRPM) subfamily members and calcium signalling processes are implicated in the neurological, immunological, cardiovascular, and metabolic impairments inherent in ME/CFS. In this review, we present TRPM7 as a potential candidate in the pathomechanism of ME/CFS, as TRPM7 is increasingly recognized as a key mediator of physiological and pathophysiological mechanisms affecting neurological, immunological, cardiovascular, and metabolic processes. A focused examination of the biochemistry of TRPM7, the role of this protein in the aforementioned systems, and the potential of TRPM7 as a molecular mechanism in the pathophysiology of ME/CFS will be discussed in this review. TRPM7 is a compelling candidate to examine in the pathobiology of ME/CFS as TRPM7 fulfils several key roles in multiple organ systems, and there is a paucity of literature reporting on its role in ME/CFS.

Suggested Citation

  • Stanley Du Preez & Helene Cabanas & Donald Staines & Sonya Marshall-Gradisnik, 2021. "Potential Implications of Mammalian Transient Receptor Potential Melastatin 7 in the Pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Review," IJERPH, MDPI, vol. 18(20), pages 1-15, October.
    • Handle: RePEc:gam:jijerp:v:18:y:2021:i:20:p:10708-:d:654686
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    References listed on IDEAS

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    1. Monica J. S. Nadler & Meredith C. Hermosura & Kazunori Inabe & Anne-Laure Perraud & Qiqin Zhu & Alexander J. Stokes & Tomohiro Kurosaki & Jean-Pierre Kinet & Reinhold Penner & Andrew M. Scharenberg & , 2001. "Erratum: LTRPC7 is a Mg·ATP-regulated divalent cation channel required for cell viability," Nature, Nature, vol. 412(6847), pages 660-660, August.
    2. Monica L Joustra & Isidor Minovic & Karin A M Janssens & Stephan J L Bakker & Judith G M Rosmalen, 2017. "Vitamin and mineral status in chronic fatigue syndrome and fibromyalgia syndrome: A systematic review and meta-analysis," PLOS ONE, Public Library of Science, vol. 12(4), pages 1-25, April.
    3. Monica J. S. Nadler & Meredith C. Hermosura & Kazunori Inabe & Anne-Laure Perraud & Qiqin Zhu & Alexander J. Stokes & Tomohiro Kurosaki & Jean-Pierre Kinet & Reinhold Penner & Andrew M. Scharenberg & , 2001. "LTRPC7 is a Mg·ATP-regulated divalent cation channel required for cell viability," Nature, Nature, vol. 411(6837), pages 590-595, May.
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