In their August American Journal of Respiratory Cell and Molecular Biology article, Dilip Shah and colleagues demonstrate that lung endothelial dysfunction in diet–induced obese (DIO) mice coincides with increased endoplasmic reticulum (ER) stress. In these mice, the researchers observed “enhanced expression of the major sensors of misfolded proteins including PERK, IREalpha, and ATF6.” They also found that lung endothelial cells exposed to serum from obese mice resulted in enhanced expression of ER stress markers.

The authors then tested whether reducing ER stress also reduced the risk of acute lung injury in these mice. They found that “treatment with 4–PBA, a chemical protein chaperone that reduces ER stress, restored vascular endothelial cell expression of adhesion molecules and protected against LPS [lipopolysaccharide]–induced acute lung injury in DIO mice.” The authors believe their findings should lead to testing similar approaches to preventing acute lung injury in obese people.

The article is titled, "Obesity–induced Endoplasmic Reticulum Stress Causes Lung Endothelial Dysfunction and Promotes Acute Lung Injury."