CCL2 and pneumonia: The possible mechanism is as follows: local inflammatory factors (such as monocyte chemoattractant protein-1) secreted by intramuscular fat and lipid toxic metabolites directly damage mitochondrial function as well as the contractility and endurance of skeletal muscles (especially the diaphragm), which leads to respiratory muscle weakness, insufficient pulmonary ventilation, and accelerated respiratory failure related to pneumonia [38,39].