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Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue
Published on: May 17, 2018
Mitochondria and immunity in chronic fatigue syndrome
G Anderson1, M Maes2
1CRC Scotland & London, Eccleston Square, London, UK.
Abstract:
It is widely accepted that the pathophysiology and treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) could be considerably improved. The heterogeneity of ME/CFS and the confusion over its classification have undoubtedly contributed to this, although this would seem a consequence of the complexity of the array of ME/CFS presentations and high levels of diverse comorbidities. This article reviews the biological underpinnings of ME/CFS presentations, including the interacting roles of the gut microbiome/permeability, endogenous opioidergic system, immune cell mitochondria, autonomic nervous system, microRNA-155, viral infection/re-awakening and leptin as well as melatonin and the circadian rhythm. This details not only relevant pathophysiological processes and treatment options, but also highlights future research directions. Due to the complexity of interacting systems in ME/CFS pathophysiology, clarification as to its biological underpinnings is likely to considerably contribute to the understanding and treatment of other complex and poorly managed conditions, including fibromyalgia, depression, migraine, and dementia. The gut and immune cell mitochondria are proposed to be two important hubs that interact with the circadian rhythm in driving ME/CFS pathophysiology.
Insights
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) involves complex biological factors like the gut microbiome and immune cell mitochondria. Understanding these interactions with the circadian rhythm is key to improving ME/CFS treatment and managing other complex conditions.
Area of Science:
- Immunology
- Neuroscience
- Microbiology
Background:
- Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) presents significant challenges in pathophysiology and treatment.
- Heterogeneity in ME/CFS presentations and high comorbidity rates complicate understanding and classification.
Purpose of the Study:
- To review the biological underpinnings of ME/CFS presentations.
- To explore potential treatment avenues and future research directions.
- To elucidate the role of interacting systems in ME/CFS pathophysiology.
Main Methods:
- Literature review of biological factors implicated in ME/CFS.
- Analysis of the interplay between the gut microbiome, immune system, and nervous system.
- Examination of molecular pathways including microRNA-155 and viral reactivation.
Main Results:
- Key biological factors include gut microbiome/permeability, opioidergic system, immune cell mitochondria, autonomic nervous system dysfunction, microRNA-155, viral activity, leptin, melatonin, and circadian rhythm.
- The gut and immune cell mitochondria are identified as critical hubs interacting with the circadian rhythm.
- Understanding these mechanisms may offer insights into treating other complex conditions like fibromyalgia and dementia.
Conclusions:
- Clarifying the biological underpinnings of ME/CFS is crucial for advancing treatment strategies.
- The gut microbiome, immune cell mitochondria, and circadian rhythm are central to ME/CFS pathophysiology.
- Further research into these interconnected systems holds promise for broader clinical applications.
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