TLR4 and serum lipopolysaccharide activity: Endotoxin was found to accelerate the diaphragm dysfunction process in ventilated rabbits and murine endotoxemia model by augmenting diaphragmatic structural damage, lipid accumulation, release of free radicals, muscle proteolysis, mitochondrial dysfunction, and autophagy of the diaphragm via the toll-like receptor 4 (TLR4)/NF-κB pathway, thus resulting in diaphragmatic contractility impairment [31, 32].