ArticleJournal of advanced research2024
Ceramide-1-phosphate alleviates high-altitude pulmonary edema by stabilizing circadian ARNTL-mediated mitochondrial dynamics.
Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 19 citations in OpenAlex.
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Lipid profile shift in high-altitude migrants as a key promoting factor for chronic myocardial injury revealed by lipidomics.Cell communication and signaling : CCS · 2026Article
- Intervention effect of small extracellular vesicles derived from dental pulp stem cells on a high-altitude pulmonary edema model in male rats.Physiological reports · 2026Article
- Paeoniflorin alleviates hypobaric hypoxia-triggered lung injury through targeting MEK2 to modulate ERK2-SGK1 signaling.Acta pharmaceutica Sinica. B · 2026Article
- High-Altitude Condition Induces Hepatic Magnetic Susceptibility Changes and Liver Injury.Biomolecules · 2026Article
- Spatiotemporal dynamics of reactive oxygen species: implications for cellular homeostasis and redox therapies.Cellular & molecular biology letters · 2026Review
- HIF-1α and BMAL1 in bone regeneration: crosstalk between hypoxia response and circadian rhythm.Bone research · 2026Review
- Transcriptomic analysis and experimental verification reveal the involvement of PI3K/AKT signaling pathway in high-altitude cognitive dysfunction.Frontiers in physiology · 2026Article
- Sphingomyelin Synthase 2 Deletion Mitigates Oxidative Stress-Induced NF-κB Activation via Lipid Metabolic Reprogramming in Dry Eye Disease.Investigative ophthalmology & visual science · 2025Article
- Acute high-altitude hypoxia induced NLRP3 inflammasome activation in pulmonary artery smooth muscle cells by BMAL1 targeting mitochondrial VDAC1-mediated MtDNA leakage.Apoptosis : an international journal on programmed cell death · 2025Article
- Trans-Sodium Crocetinate Ameliorates High-Altitude Acute Lung Injury via Modulating EGFR/PI3K/AKT/NF-κB Signaling Axis.Nutrients · 2025Article
- Sphingolipid metabolites involved in the pathogenesis of atherosclerosis: perspectives on sphingolipids in atherosclerosis.Cellular & molecular biology letters · 2025Review
- 7-Hydroxyethyl Chrysin Alleviates High Altitude Pulmonary Edema via Activation of the PI3K/AKT Signaling Pathway.Drug design, development and therapy · 2025Article
- 6-Hydroxygenistein Ameliorates High Altitude Brain Injury via Activating PI3K/AKT Signaling Pathway Based on Transcriptomic Analysis and Experimental Validation.Drug design, development and therapy · 2025Article
- Whole transcriptome landscape in HAPE under the stress of environment at high altitudes: new insights into the mechanisms of hypobaric hypoxia tolerance.Frontiers in immunology · 2024Article
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionHigh-altitude pulmonary edema (HAPE) is a severe and potentially fatal condition with limited treatment options. Although ceramide kinase (CERK)-derived ceramide-1-phosphate (C1P) has been demonstrated to offer protection against various pulmonary diseases, its effects on HAPE remain unclear.
objectivesOur study aimed to investigate the potential role of CERK-derived C1P in the development of HAPE and to reveal the molecular mechanisms underlying its protective effects. We hypothesized that CERK-derived C1P could protect against HAPE by stabilizing circadian rhythms and maintaining mitochondrial dynamics.
methodsTo test our hypothesis, we used CERK-knockout mice and established HAPE mouse models using a FLYDWC50-1C hypobaric hypoxic cabin. We utilized a range of methods, including lipidomics, transcriptomics, immunofluorescence, Western blotting, and transmission electron microscopy, to identify the mechanisms of regulation.
resultsOur findings demonstrated that CERK-derived C1P played a protective role against HAPE. Inhibition of CERK exacerbated HAPE induced by the hypobaric hypoxic environment. Specifically, we identified a novel mechanism in which CERK inhibition induced aryl hydrocarbon receptor nuclear translocator-like (ARNTL) autophagic degradation, inducing the circadian rhythm and triggering mitochondrial damage by controlling the expression of proteins required for mitochondrial fission and fusion. The decreased ARNTL caused by CERK inhibition impaired mitochondrial dynamics, induced oxidative stress damage, and resulted in defects in mitophagy, particularly under hypoxia. Exogenous C1P prevented ARNTL degradation, alleviated mitochondrial damage, neutralized oxidative stress induced by CERK inhibition, and ultimately relieved HAPE.
conclusionsThis study provides evidence for the protective effect of C1P against HAPE, specifically, through stabilizing circadian rhythms and maintaining mitochondrial dynamics. Exogenous C1P therapy may be a promising strategy for treating HAPE. Our findings also highlight the importance of the circadian rhythm and mitochondrial dynamics in the pathogenesis of HAPE, suggesting that targeting these pathways may be a potential therapeutic approach for this condition.
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