JAK/STAT inhibition augments soleus muscle function in a rat model of critical illness myopathy via regulation of complement C3/3R

Key points Critical illness myopathy (CIM) is a frequently observed negative consequence of modern critical care. Chronic Janus kinase (JAK)/signal transducer and activator transcription activation impairs muscle size function prominent following mechanical ventilation. We identify pSTAT-3 in tibialis anterior CIM patients, before examining the potential benefits JAK1/2 inhibition an experimental model CIM, where mass are impaired. activates complement cascade increased monocyte infiltration soleus muscle, which was ameliorated by inhibition, leading to reduced degeneration improved force. Here, we demonstrate that augments through regulation cascade. Abstract response care with consequences for patient quality life, morbidity, mortality healthcare costs. (STAT) limb muscles controlled JAK/STAT promotes loss function. Thus, hypothesized would improve outcomes CIM. Following 12 days intensive unit conditions, levels patients (P = 0.0489). The assessed force restores < 0.0001). activated cascade, 0.05, respectively). Soleus macrophage number corresponded activity, augmented 0.05). improves modulating infiltration. Collectively,