ArticleCurrent pharmaceutical design2025
Esketamine Regulates Mitophagy through ULK1/FUNDC1 Signaling Pathway to Improve LPS-induced Acute Respiratory Distress Syndrome.
Article in Current pharmaceutical design, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Effects of Esketamine-Dexmedetomidine Combination on Immediate Postprocedural Oxygenation Index in Severe Pneumonia Patients Undergoing Bedside Fiberoptic Bronchoscopic Sputum Aspiration: A Prospective Randomised Controlled Trial.Drug design, development and therapy · 2025Trial
- Mitophagy in pathogenesis and therapeutic implications for infection.Experimental & molecular medicine · 2026Review
- Sedation as an Immunomodulator of Inflammatory Responses in the Lung-Brain Axis of ARDS.International journal of molecular sciences · 2026Review
- Esketamine alleviates COPD-depression comorbidity in rats via MAPK/NF-κB inhibition and gut-lung-brain axis modulation.Journal of neuroinflammation · 2026Article
- New Exploration of Therapeutic Targets for Radiation Pneumonitis: Comparative Analysis of Molecular Pathways in Radiation-Induced and LPS-Induced Pneumonitis.International journal of medical sciences · 2025Review
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAs a heterogeneous clinical syndrome, acute respiratory distress syndrome (ARDS) is caused by infection-associated inflammation with limited treatment options. Esketamine possesses antiinflammatory properties, and it is effective in treating lung diseases.
objectiveThis study aimed to unveil the efficacy and mechanism of esketamine in ARDS.
methodsLipopolysaccharide (LPS) is widely used to induce inflammatory response in lung injury. The mice model of ARDS in this study was established through the inhalation of LPS. Hematoxylin-eosin (H&E) staining was used to evaluate the pathological changes in the lung tissues of ARDS mice, and the histological index of lung damage was employed. Bicinchoninic acid (BCA) assay kits were utilized to assess the total proteins in bronchoalveolar lavage fluid (BALF), and a hemocytometer was used to count the number of total cells. The pulmonary vascular permeability was detected using Evans blue staining. Western blot was carried out to detect the expressions of tight junction proteins, and enzyme-linked immunosorbent assay (ELISA) detected the release of inflammatory cytokines in BALF and serum. Dihydroethidium (DHE) staining was used to detect reactive oxygen species (ROS) production, and the levels of myeloperoxidase (MPO) and oxidative stress markers were measured using corresponding assay kits. Apoptosis was assessed through terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and Western blot. Immunostaining detected the FUN14 domain-containing 1 (FUNDC1) and light chain 3B (LC3B) in lung tissues, and the expressions of autophagy-related proteins were detected using Western blot.
resultsOur data showed that esketamine treatment alleviated LPS-stimulated lung damage, improved pulmonary vascular permeability, and inhibited inflammatory response, oxidative stress, and apoptosis in ARDS mice. Mechanically, esketamine activated mitophagy through UNC-52-like kinase 1 (ULK1)/FUNDC1 signaling pathway. These findings, for the first time, revealed the therapeutic potential of esketamine in treating ARDS.
conclusionCollectively, this study revealed the protective role of esketamine against lung injury, inflammation, oxidative stress, and apoptosis in mice with ARDS and revealed the reaction mechanism related to mitophagy.
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