Journal Article Review Epublish
PubMed: 40149893 DOI: 10.3390/biom15030357
Unravelling the Connection Between Energy Metabolism and Immune Senescence/Exhaustion in Patients with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.
Biomolecules 15(3)
Authors: Jente Van Campenhout, Yanthe Buntinx, Huan-Yu Xiong, Arne Wyns, Andrea Polli, Jo Nijs, Joeri L Aerts, Thessa Laeremans, Jolien Hendrix
Affiliations
- Pain in Motion Research Group (PAIN), Department of Physiotherapy, Human Physiology and Anatomy, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium.
- Flanders Research Foundation-FWO, 1090 Brussels, Belgium.
- Department of Public Health and Primary Care, Centre for Environment & Health, KU Leuven, Kapucijnenvoer 35, 3000 Leuven, Belgium.
- Unit of Physiotherapy, Department of Health and Rehabilitation, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, SE-405 30 Gothenburg, Sweden.
- Department of Physical Medicine and Physiotherapy, University Hospital Brussels, 1090 Brussels, Belgium.
- Laboratory of Neuro-Aging & Viro-Immunotherapy, Center for Neurosciences, Vrije Universiteit Brussel (VUB), Laarbeeklaan 103, 1090 Brussels, Belgium.
Abstract
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating disease, characterized by a diverse array of symptoms including post-exertional malaise (PEM), severe fatigue, and cognitive impairments, all of which drastically diminish the patients' quality of life. Despite its impact, no curative treatments exist, largely due to the limited understanding of the disease's underlying pathophysiology. Mitochondrial dysfunction, leading to impaired energy production and utilization, is believed to play a key role in the onset of fatigue and PEM, positioning it as a potential key pathophysiological mechanism underlying ME/CFS. Additionally, the disorder shows similarities to chronic viral infections, with frequent reports of immune system alterations, suggesting a critical role for immune (dys)functioning. In particular, the roles of immune senescence and immune exhaustion-two fundamental immune states-remain poorly understood in ME/CFS. This state-of-the-art review explores how metabolic dysfunction and immune dysfunction may be interconnected in ME/CFS, proposing that energy deficits may directly impair immune function. By examining this metabolic-immune interplay, this review highlights potential pathways for developing innovative therapeutic strategies that target both energy metabolism and immune regulation, offering hope for improving patient outcomes.
MeSH
Killer Cells, Natural, Encephalomyelitis, Pain, Fatigue Syndrome, Chronic, Biomarkers, Fatigue, Therapeutics