ArticleTranslational pediatrics2025
Szeto-Schiller 31 eases acute lung injury in neonatal mice with acute respiratory distress syndrome by mediating TXNIP expression and NLRP3 inflammasome activation.
Article in Translational pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Cuproptosis of bronchial epithelial cells triggers airway remodeling in chronic asthma.Scientific reports · 2026Article
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7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Mitochondrial-targeting anti-oxidant Szeto-Schiller 31 (SS-31) can ease lung injury in several diseases, but whether SS-31 can ameliorate acute lung injury (ALI) in neonatal acute respiratory distress syndrome (ARDS) is unclear. The objective of this study is to explore the efficacy of SS-31 against ALI and the associated molecular mechanisms. Methods: Thioredoxin-interacting protein (TXNIP) was found to be a hub gene for ARDS by bioinformatics analysis. Using the Search Tool for Interactions of Chemicals (STITCH) database, SS-31 was found to work via mediating TXNIP expression. Serum levels of some parameters were analyzed by enzyme-linked immunosorbent assay (ELISA). The effect of SS-31 on oxidative stress (OxS) injury, inflammation, apoptosis, and vascular permeability in lipopolysaccharide (LPS)-induced human lung microvascular epithelial cells (HLMVECs) and ARDS mouse models were investigated to assess the efficiency of SS-31 on ALI by a series of experiments [5-ethynyl-2'-deoxyuridine (EDU), lactate dehydrogenase (LDH), western blot, flow cytometry, histopathological analysis, wet-to-dry weight ratio, and so on]. Results: SS-31 treatment mitigated LPS-induced OxS, apoptosis, vascular permeability, and inflammatory response in HLMVECs. Consistently, SS-31 treatment ameliorated histopathological changes and oedema in the lungs of neonatal ARDS mice, accompanied by improved alveolar capillary barrier integrity as well as reduced OxS, inflammation, and apoptosis. Serum TXNIP, caspase-1, apoptosis-associated speck-like protein (ASC), and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) levels were overtly higher in newborns with ARDS, and a positive correlation was observed between TXNIP and NLRP3. Interestingly, SS-31 treatment repressed TXNIP and NLRP3 protein levels in ARDS cells and animal models. Conclusions: SS-31 may repress OxS, inflammatory response, apoptosis, and vascular permeability by targeting the TXNIP/NLRP3 pathway in neonatal ARDS, thereby ameliorating ALI.
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