For a study, researchers sought to examine the association between myostatin, a muscle protein, plasma levels, and acquired weakness in Intensive care unit-acquired weakness (ICUAW). Clinical and/or pathophysiological considerations were taken into account when examining the possibility of therapeutic myostatin inhibition. Investigators evaluated the dynamics of myostatin plasma concentrations (days 4, 8, and 14) and myostatin gene (MSTN) expression levels in skeletal muscle in retrospective research using pooled data from 2 prospective studies (day 15). They investigated the connections between myostatin, muscle metabolism, atrophy-inducing pathways, and clinical and electrophysiological consequences. All critically ill patients had significantly lower levels of myostatin plasma concentrations and MSTN gene expression when compared to healthy controls (median [IQR] fold change: 1.00 [0.68-1.54] vs. 0.26 [0.11-0.80]; P=0.004). In patients with severe illnesses, myostatin plasma concentrations increased throughout time (median [IQR] fold change: day 4: 0.13 [0.08/0.21], day 8: 0.23 [0.10/0.43], day 14: 0.40 [0.26/0.61; P<0.001). ICUAW patients had significantly lower levels of MSTN gene expression than non-ICUAW patients (median [IQR] fold change: 0.17 [0.10/0.33] and 0.51 [0.20/0.86]; P=0.047). The insulin sensitivity index and muscular strength were both favorably correlated with myostatin levels (correlation coefficient 0.339, P=0.020). Myostatin plasma concentrations, MSTN expression levels, mobilization levels, electrophysiological characteristics, or indicators of atrophy pathways were not correlated. During severe sickness, myostatin protein levels and muscle gene expression were downregulated. Therefore, it did not appear to be a pathophysiological basis for the previously suggested therapeutic decrease of myostatin to enhance muscle quality in critically ill patients.
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