Abstract
Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is a disabling condition of unknown cause having multi-system manifestations. Our group has investigated the potential role of transient receptor potential (TRP) ion channels in the etiology and pathomechanism of this illness. Store-operated calcium entry (SOCE) signaling is the primary intracellular calcium signaling mechanism in non-excitable cells and is associated with TRP ion channels. While the sub-family (Canonical) TRPC has been traditionally associated with this important cellular mechanism, a member of the TRPM sub-family group (Melastatin), TRPM3, has also been recently identified as participating in SOCE in white matter of the central nervous system. We have identified single nucleotide polymorphisms (SNPs) in TRP genes in natural killer (NK) cells and peripheral blood mononuclear cells (PBMCs) in CFS/ME patients. We also describe biochemical pathway changes and calcium signaling perturbations in blood cells from patients. The ubiquitous distribution of TRP ion channels and specific locations of sub-family group members such as TRPM3 suggest a contribution to systemic pathology in CFS/ME.
Highlights
We have demonstrated that dysregulation of transient receptor potential (TRP) receptors, in particular, TRPM3, results in disturbed Ca2+ signaling and downstream kinase and gene transcription events in Chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME)
In the study of single nucleotide polymorphisms (SNPs) in B cells, Marshall-Gradisnik et al reported 78 SNPs were identified in nicotinic and muscarinic acetylcholine (ACh) receptor genes in CFS/ME, of which 35 were in muscarinic ACh receptor 3. We suggest these SNPs may be involved in B cell functional changes, indicating a role for Ca2+ dysregulation in ACh receptors and TRP ion channel signaling in the pathomechanism of CFS/ME
CFS/ME is a complex and highly disabling condition associated with central nervous system (CNS) and metabolic symptoms including memory and concentration impairment, widespread pain, and profound fatigue characterized by post-exertional malaise
Summary
CFS/ME exhibits neurological, endocrine, autonomic, metabolic, and immunological manifestations [1]. Chemical and food intolerances are notable, and patients commonly report exacerbation of symptoms with infections. In this brief review, we discuss the role of transient receptor potential (TRP) ion channels in neurological and metabolic systems in CFS/ME patients possibly contributing to the clinical expression of the illness. The aim of this paper is to understand the potential role of TRP ion channels in the etiology and pathomechanism of CFS/ME. Future research may help identify suitable pathways amenable to pharmaco-therapeutic interventions
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