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Collectively, these early alterations in inflammatory responses and neurobiochemical markers were highly consistent with the severe skeletal muscle atrophy, mitochondrial structural damage, neuromuscular junction disruption, and decreased muscle strength observed at the experimental endpoint, thereby uncovering a clear pathophysiological temporal cascade: early-onset and progressively aggravating systemic inflammation serves as the initiating factor for SAW, which subsequently drives the progressive aggravation of skeletal muscle morphological and functional impairments during disease progression
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