Caveolin-1 identified as a key mediator of acute lung injury using bioinformatics and functional research.

Acute lung injury (ALI) is a potentially life-threatening, devastating disease with an extremely high rate of mortality. The underlying mechanism of ALI is currently unclear. In this study, we aimed to confirm the hub genes associated with ALI and explore their functions and molecular mechanisms using bioinformatics methods.

Glycyrrhizic Acid Alleviates Lipopolysaccharide (LPS)-Induced Acute Lung Injury by Regulating Angiotensin-Converting Enzyme-2 (ACE2) and Caveolin-1 Signaling Pathway.

Acute lung injury (ALI) is mainly caused by severe infection, shock, trauma, and burn, which causes the extensive release of inflammatory factors and other mediators. As a major bioactive constituent of traditional Chinese herb licorice, glycyrrhizic acid (GA) plays an important effect on inflammatory regulation. Nevertheless, the exact mechanism of this effect remains unclear.

Glycyrrhizic acid ameliorates LPS-induced acute lung injury by regulating autophagy through the PI3K/AKT/mTOR pathway.

Acute lung injury (ALI) is a major pathological issue characterized by serious inflammatory response, and a major clinically critical illness with high morbidity and mortality. Glycyrrhizic acid (GA) is a major bioactive constituent isolated from traditional Chinese herb licorice, which has been reported to have positive effects on inflammation. Nevertheless, the effects of GA on lipopolysaccharide (LPS)-treated ALI in mice have not been reported.

High-Mobility Group Box 1 (HMGB1) and Autophagy in Acute Lung Injury (ALI): A Review.

Acute lung injury (ALI) is a life-threatening clinical syndrome in critically ill patients. The identification of novel biological markers for the early diagnosis of ALI and the development of more effective treatments are topics of current research. High mobility group box-1 protein (HMGB1) is a late inflammatory mediator associated with sepsis, malignancy, and immune disease.