Mughal, Sheeza, Andújar-Sánchez, Félix, Sabater-Arcis, Maria et al. · Biofabrication · 2025 · DOI
Researchers grew human muscle tissue in the laboratory and exposed it to blood from ME/CFS and Long COVID patients to see what happens. They found that muscle exposed to patient blood initially tries to work harder by burning more fuel, but over time the muscle becomes weak and fragile. The mitochondria (the energy-producing structures in cells) also change shape and stop working properly, suggesting the muscle is struggling under stress.
This is the first laboratory model demonstrating how ME/CFS patient blood may directly damage skeletal muscle tissue, potentially explaining the muscle weakness and post-exertional malaise many patients experience. Understanding this mechanism could lead to new diagnostic tests and targeted treatments for muscle dysfunction in ME/CFS and Long COVID. The findings suggest that the problem originates in circulating blood factors rather than the muscle itself, opening new therapeutic avenues.
This study does not prove that the factors in patient sera are the sole cause of ME/CFS muscle symptoms in actual patients, nor does it identify which specific blood components are responsible for the damage. The in vitro model, while valuable, does not fully replicate the complex biological environment of the human body, so these findings require confirmation in patient studies. Correlation between serum exposure and muscle changes does not establish causation in the living organism.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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