Decoding Chronic Fatigue: The Crucial Role of WASF3 in Mitochondrial Dysfunction in ME/CFS

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News Release, World Mitochondria Society, Berlin - Germany – August 15, 2023

A significant study was reported in the Proceedings of the National Academy of Sciences yesterday, shedding new light on the molecular mechanisms underlying chronic fatigue and strategic role of mitochondria. Here are the main takeaways from the study:

Main Finding

In myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a protein called WASF3, induced by endoplasmic reticulum (ER) stress, detrimentally affects mitochondrial functions, resulting in exercise intolerance.

Patient Case

In a detailed examination of a 38-year-old woman suffering from chronic fatigue, an overexpression of WASF3 was identified. This overexpression is linked to a disruption in the formation of mitochondrial respiratory supercomplexes.

Mouse Model Insights

  • Mice with heightened WASF3 levels exhibited reduced exercise capabilities.
  • A clear association was observed between elevated WASF3 levels and compromised mitochondrial functionality in skeletal muscles.

Mitigation Strategy

The study suggests a potential intervention. By diminishing ER stress, WASF3 levels were reduced, leading to a noticeable improvement in mitochondrial function.

Extended Research

Further corroborating the primary findings, muscle biopsies from a wider group of ME/CFS patients also presented elevated WASF3 levels, coupled with signs of aberrant ER stress activation.

Broader Implications

Beyond the primary focus on ME/CFS, the findings from this research provide valuable insights that could inform understanding of other fatigue-related disorders. This includes conditions like rheumatic diseases and the emerging concerns surrounding long COVID.

This study marks a pivotal step forward in understanding the intricacies of chronic fatigue at the molecular level, offering hope for improved diagnostic and therapeutic approaches in the future.

Article DOI.


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