Abstract
Acute lung injury is featured as diffuse pulmonary edema and persistent hypoxemia caused by lung or systemic injury. It is believed that these pathological changes are associated with damage to the alveolar epithelium and vascular endothelium, recruitment of inflammatory cells, and inflammatory factor storms. In recent years, the metabolic reprogramming of lung parenchymal cells and immune cells, particularly alterations in glycolysis, has been found to occur in acute lung injury. Inhibition of glycolysis can reduce the severity of acute lung injury. Thus, this review focuses on the interconnection between acute lung injury and glycolysis and the mechanisms of interaction, which may bring hope for the treatment of acute lung injury.
Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
