Cayman's Cellular Metabolism expert in collaboration with University of Michigan researchers offers an insightful review of the cellular and mitochondrial implications of this debilitating disease and the identification of multiple targets for potential pharmacological intervention.

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic disease characterized by debilitating fatigue that is not alleviated by rest. Current therapeutic options are largely limited to palliative care and cognitive management because the mechanistic basis of the disease is poorly understood. Viral infection is a known trigger for ME/CFS. Thus, the ongoing COVID-19 pandemic may increase ME/CFS prevalence as some COVID long-hauler experiences are similar to that of ME/CFS patients. Here is the current understanding of the causes of ME/CFS:

• One hypothesis suggests that ME/CFS results from an aberrant or misdirected immune reaction to an initial infection that has progressed into a chronic autoimmune disease.

• Other evidence indicates immune dysregulation in ME/CFS that impairs natural killer cell function, increases B cell and activated CD8⁺ T cells, and alters cytokine levels.
  

• Additional analyses reveal that multiple metabolic pathways have decreased function in ME/CFS, pointing toward mitochondrial dysfunction (increased mitochondrial damage, reduced ATP production, and impaired oxidative phosphorylation).

This article reviews these factors and potential biomarkers to detect these immune and metabolic irregularities as well as discusses current and experimental approaches to therapies that target key aspects of the immune system and mitochondrial metabolism.

Toogood, P.L., Clauw, D.J., Phadke, S., Hoffman, D. Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): Where will the drugs come from? Pharmacol. Res. 105465 (2021).

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