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However, in patients with PEM, due to underlying pathological factors, such as persistent viral infections, mitochondrial autophagy and repair mechanisms are impaired, hindering the effective resolution of mitochondrial stress and initiating a potential pathological feedback loop ( 2.2 Decline in ATP synthesis and insufficient energy supply The traditional view asserts that the marked decline in ATP synthesis resulting from mitochondrial dysfunction is a potential primary contributor to the muscle weakness and fatigue observed in PEM (68, 69)