Impairment of Fatty Acid Oxidation in Alveolar Epithelial Cells Mediates Acute Lung Injury.

ABSTRACT: Profound impairment in cellular oxygen consumption, referred to as cytopathic dysoxia, is one of the pathological hallmarks in the lungs of patients with pathogen-induced acute lung injury (ALI). However, the underlying mechanism for this functional defect remains largely unexplored. In this study, we found that primary mouse alveolar epithelial cells (AECs) conducted robust fatty acid oxidation (FAO). More importantly, FAO was strikingly impaired in AECs of mice with LPS-induced ALI. The metabolic deficiency in these cells was likely due to decreased expression of key mediators involved in FAO and mitochondrial bioenergenesis, such as peroxisome proliferator-activated receptor γ coactivator (PGC)-1α, carnitine palmitoyltransferase 1A, and medium-chain acyl-CoA dehydrogenase (CAD). We foun

SUBMITTER: Cui H 

PROVIDER: S-EPMC6376408 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature