Autophagy, TERT, and mitochondrial dysfunction in hyperoxia
Andreas Beyer, Laura E. Norwood Toro, William E. Hughes, Micaela Young, Anne V. Clough, Feng Gao, Meetha Medhora, Said H. Audi, Elizabeth R. Jacobs
Abstract
In cultured pulmonary artery endothelial cells and in lungs exposed in vivo to hyperoxia, autophagy is activated, but clearance of autophagosomes is impaired in a manner that suggests cross talk between TERT and autophagy. Stimulation of autophagy prevents hyperoxia-induced decreases in mitochondrial metabolism and sustains monolayer resistance. Hyperoxia increases mitochondrial outer membrane (TOMM20) protein, decreases mitochondrial function, and reduces cellular proliferation without increasing cell death.
Topics & Concepts
HyperoxiaAutophagyCell biologyMitochondrionProgrammed cell deathStimulationBiologyMitophagyReactive oxygen speciesIn vivoChemistryApoptosisLungInternal medicineMedicineEndocrinologyBiochemistryBiotechnologyAutophagy in Disease and TherapyMitochondrial Function and PathologySulfur Compounds in Biology