2022
DOI: 10.3389/fphar.2022.762840
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Abstract: Acute lung injury (ALI) and its severe manifestation, acute respiratory distress syndrome (ARDS), are treated with high concentrations of supplementary oxygen. However, prolonged exposure to high oxygen concentrations stimulates the production of reactive oxygen species (ROS), which damages the mitochondria and accumulates misfolded proteins in the endoplasmic reticulum (ER). The mitochondrial protein A-kinase anchoring protein 1 (Akap1) is critical for mitochondrial homeostasis. It is known that Akap1 deficie… Show more

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Cited by 4 publications
(3 citation statements)
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“…In this study, Akt phosphorylation was analyzed only at Ser473. Further, Akap1 deletion and oxidant injury exacerbates ER stress in mice ( Sidramagowda Patil et al, 2022 ). This suggests that the ER stress in Akap1 −/− mice exposed to hyperoxia may induce phosphorylation of Ser473 via GRP78 and, in turn, defines Akt target specificities ( Yung et al, 2011 ).…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…In this study, Akt phosphorylation was analyzed only at Ser473. Further, Akap1 deletion and oxidant injury exacerbates ER stress in mice ( Sidramagowda Patil et al, 2022 ). This suggests that the ER stress in Akap1 −/− mice exposed to hyperoxia may induce phosphorylation of Ser473 via GRP78 and, in turn, defines Akt target specificities ( Yung et al, 2011 ).…”
Section: Discussionmentioning
confidence: 99%
“…In 2018, our group demonstrated that Akap1 −/− mice exposed to 48 h of hyperoxia display ALI, characterized by increases in pro-inflammatory cytokines, edema, inflammatory immune cells, aberrant mitochondria, and autophagy and mitophagy ( Narala et al, 2018 ). Further, Akap1 −/− mice subjected to oxidant injury exhibit higher expression of ER stress markers including binding immunoglobulin protein 1 (Bip1), C/EBP Homologous protein (CHOP), eIF2α phosphorylation, JNK phosphorylation and ER stress-induced autophagy ( Sidramagowda Patil et al, 2022 ).…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, treatment with ER-stress inhibitor 4-phenyl butyric acid protects against hyperoxic-cell death both in vivo and in vitro (Pao et al 2021 ). Recent evidence showed role of the mitochondrial protein A-kinase anchoring protein 1 (Akap1) and ER stress in protection against hyperoxia; deletion of Akap1 resulted in increased ER stress-associated cell death (Sidramagowda Patil et al 2022 ).…”
Section: Hyperoxia Causes Cell Death Via Multiple Pathwaysmentioning
confidence: 99%