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Obesity and ALI: What’s the Link and How Might It Be Broken?

August 2, 2017 at 3:03 pm

By Paul Schumacker, PhD, editor, American Journal of Respiratory Cell and Molecular Biology

Follow Dr. Schumacker on Twitter @AJRCMB

Obesity-induced Endoplasmic Reticulum Stress Causes Lung Endothelial Dysfunction and Promotes Acute Lung Injury

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, IREα, 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.

August Highlights

Foxp3+ Regulatory T Cell Expression of Keratinocyte Growth Factor Enhances Lung Epithelial Proliferation

Runt-Related Transcription Factor 1 Regulates LPS-Induced Acute Lung Injury via NF-κB Signaling

Gene Expression Analysis to Assess the Relevance of Rodent Models to Human Lung Injury

Integrated Stress Response Mediates Epithelial Injury in Mechanical Ventilation

Glucocorticoid Receptor ChIP-seq Identifies PLCD1 as a KLF15 Target that Represses Airway Smooth Muscle Hypertrophy

Efficiency and Specificity of Gene Deletion in Lung Epithelial Doxycycline-Inducible Cre Mice


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