ArticlePloS one2016
Deletion of ASK1 Protects against Hyperoxia-Induced Acute Lung Injury.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Advances in research on hyperoxia-induced acute lung injury: from pathogenesis to therapy.Frontiers in cell and developmental biology · 2026Review
- Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.Frontiers in physiology · 2025Article
- Oxidative stress in ARDS: mechanisms and therapeutic potential.Frontiers in pharmacology · 2025Review
- Signaling pathways and potential therapeutic targets in acute respiratory distress syndrome (ARDS).Respiratory research · 2024Review
- Genes That Extend Lifespan May Do So by Mitigating the Increased Risk of Death Posed by Having Hypertension.American journal of hypertension · 2023Article
- Epidermal Growth Factor Receptor Inhibition Is Protective in Hyperoxia-Induced Lung Injury.Oxidative medicine and cellular longevity · 2022Article
- Article
- Hyperoxia and Lungs: What We Have Learned From Animal Models.Frontiers in medicine · 2021Review
- MicroRNA-23a-5p Is Involved in the Regulation of Lipopolysaccharide-Induced Acute Lung Injury by Targeting HSP20/ASK1.Oxidative medicine and cellular longevity · 2021Article
- Alda-1 Attenuates Hyperoxia-Induced Acute Lung Injury in Mice.Frontiers in pharmacology · 2020Article
- Apoptosis signal-regulating kinase-1 promotes inflammasome priming in macrophages.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- A mitochondrial delicacy: dynamin-related protein 1 and mitochondrial dynamics.American journal of physiology. Cell physiology · 2018Review
- Oxymatrine Causes Hepatotoxicity by Promoting the Phosphorylation of JNK and Induction of Endoplasmic Reticulum Stress Mediated by ROS in LO2 Cells.Molecules and cells · 2018Article
- Akap1 genetic deletion increases the severity of hyperoxia-induced acute lung injury in mice.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Thioredoxin-1 Protects Bone Marrow-Derived Mesenchymal Stromal Cells from Hyperoxia-Induced Injury In Vitro.Oxidative medicine and cellular longevity · 2018Article
- DNA Repair Interacts with Autophagy To Regulate Inflammatory Responses to Pulmonary Hyperoxia.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- 4-Hydroxy-2-nonenal: a critical target in oxidative stress?American journal of physiology. Cell physiology · 2016Review
- SOCS-1 rescues IL-1β-mediated suppression of epithelial sodium channel in mouse lung epithelial cells via ASK-1.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis signal-regulating kinase 1 (ASK1), a member of the MAPK kinase kinase kinase (MAP3K) family, is activated by various stimuli, which include oxidative stress, endoplasmic reticulum (ER) stress, calcium influx, DNA damage-inducing agents and receptor-mediated signaling through tumor necrosis factor receptor (TNFR). Inspiration of a high concentration of oxygen is a palliative therapy which counteracts hypoxemia caused by acute lung injury (ALI)-induced pulmonary edema. However, animal experiments so far have shown that hyperoxia itself could exacerbate ALI through reactive oxygen species (ROS). Our previous data indicates that ASK1 plays a pivotal role in hyperoxia-induced acute lung injury (HALI). However, it is unclear whether or not deletion of ASK1 in vivo protects against HALI. In this study, we investigated whether ASK1 deletion would lead to attenuation of HALI. Our results show that ASK1 deletion in vivo significantly suppresses hyperoxia-induced elevation of inflammatory cytokines (i.e. IL-1β and TNF-α), cell apoptosis in the lung, and recruitment of immune cells. In summary, the results from the study suggest that deletion of ASK1 in mice significantly inhibits hyperoxic lung injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.