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Article Synopsis
  • The study investigates how altered levels of O-GlcNAc influence damage to alveolar type II cells under hyperoxia, linking it to bronchopulmonary dysplasia (BPD).
  • Researchers treated RLE-6TN cells with inhibitors and metabolic donors to assess changes in cell viability, metabolism, and apoptosis caused by hyperoxia.
  • Findings indicate that reduced O-GlcNAc levels contribute to cell injury, while inhibiting its synthesis may protect against hyperoxia-induced damage and improve cell function.
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