4.7 Review

A systematic review of mitochondrial abnormalities in myalgic encephalomyelitis/chronic fatigue syndrome/systemic exertion intolerance disease

期刊

JOURNAL OF TRANSLATIONAL MEDICINE
卷 18, 期 1, 页码 -

出版社

BMC
DOI: 10.1186/s12967-020-02452-3

关键词

Myalgic Encephalomyelitis; Chronic Fatigue Syndrome; Systemic Exertion Intolerance Disease; Mitochondria; Energy metabolism

资金

  1. Stafford Fox Medical Research Foundation
  2. Mason Foundation
  3. Blake Beckett Foundation
  4. Alison Hunter Memorial Foundation
  5. McCusker Charitable Foundation
  6. Buxton Foundation
  7. Henty Community
  8. Henty Lions Club
  9. Change for ME Charity

向作者/读者索取更多资源

Background Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) or Systemic Exertion Intolerance Disease (SEID) present with a constellation of symptoms including debilitating fatigue that is unrelieved by rest. The pathomechanisms underlying this illness are not fully understood and the search for a biomarker continues, mitochondrial aberrations have been suggested as a possible candidate. The aim of this systematic review is to collate and appraise current literature on mitochondrial changes in ME/CFS/SEID patients compared to healthy controls. Methods Embase, PubMed, Scopus and Medline (EBSCO host) were systematically searched for articles assessing mitochondrial changes in ME/CFS/SEID patients compared to healthy controls published between January 1995 and February 2020. The list of articles was further refined using specific inclusion and exclusion criteria. Quality and bias were measured using the Joanna Briggs Institute Critical Appraisal Checklist for Case Control Studies. Results Nineteen studies were included in this review. The included studies investigated mitochondrial structural and functional differences in ME/CFS/SEID patients compared with healthy controls. Outcomes addressed by the papers include changes in mitochondrial structure, deoxyribonucleic acid/ribonucleic acid, respiratory function, metabolites, and coenzymes. Conclusion Based on the included articles in the review it is difficult to establish the role of mitochondria in the pathomechanisms of ME/CFS/SEID due to inconsistencies across the studies. Future well-designed studies using the same ME/CFS/SEID diagnostic criteria and analysis methods are required to determine possible mitochondrial involvement in the pathomechanisms of ME/CFS/SEID.

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