Burn injuries cause severe muscle wasting and weakness. However, the relative contribution of neuromuscular junction (NMJ) degradation remains elusive. We investigated the associations of plasma c-terminal agrin fragment-22 (CAF22), a marker of NMJ degradation, with muscle decline in burn patients. We recruited male
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Burn injuries cause severe muscle wasting and weakness. However, the relative contribution of neuromuscular junction (NMJ) degradation remains elusive. We investigated the associations of plasma c-terminal agrin fragment-22 (CAF22), a marker of NMJ degradation, with muscle decline in burn patients. We recruited male patients with burns (
n = 32, age = 32.3 ± 4.5 years, percent burn area = 15.2 ± 2.3) and age-matched controls to evaluate handgrip strength (HGS), skeletal muscle mass index (SMI), phase angle, and creatine kinase and plasma levels of CAF22, c-reactive protein, and 8-isoprostanes. We used an unpaired
t-test and regression analysis for statistics. The burn patients had lower HGS, SMI, and phase angle than the controls (all
p < 0.05). These patients also exhibited higher plasma CAF22, CRP, 8-isoprostanes, and creatine kinase than the controls (all
p < 0.05), suggesting NMJ degradation and heightened inflammation and oxidative stress. Correlation analysis revealed significant correlations of plasma CAF22 with HGS and phase angle in the burn patients, suggesting the potential contributions of NMJ degradation to muscle weakness and atrophy (both
p < 0.05). We also found correlations of plasma CRP with HGS and phase angle in these patients (both
p < 0.05). Altogether, NMJ degradation appears to play a significant role in burn-induced muscle injury and may warrant further investigation for potential therapeutic interventions.
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