PM2.5 exposure causes lung injury by triggering oxidative stress, mitochondrial dysfunction, and modulating HIF-1α signaling. Calcitriol activates VDR, which regulates cellular homeostasis. This study evaluated the protective role of the calcitriol/VDR system in PM2.5-induced damage to BEAS-2B bronchial epithelial cells by reducing oxidative stress, upregulating mitochondrial bioenergetics, and downregulating HIF-1α. We found that the calcitriol/VDR system decreased ROS formation and restored mitochondrial bioenergetics in PM2.5-treated cells. This improvement correlated with reduced HIF-1α nuclear translocation and increased PGC-1α protein and mitochondrial gene expressions. This study is the first to suggest that targeting the calcitriol/VDR system could be a promising pharmacological strategy for mitigating PM2.5-induced lung epithelial damage by promoting mitochondrial bioenergetics and regulating PGC-1α and HIF-1α signaling.

中文翻译：

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骨化三醇/维生素 D 受体系统通过上调线粒体生物能量学和调节 HIF-1α/PGC-1α 信号传导来减轻 PM2.5 诱导的人支气管上皮损伤


PM2.5 暴露通过触发氧化应激、线粒体功能障碍和调节 HIF-1α 信号传导导致肺损伤。骨化三醇激活 VDR，从而调节细胞稳态。本研究通过减少氧化应激、上调线粒体生物能量学和下调 HIF-1α，评估了骨化三醇/VDR 系统在 PM2.5 诱导的 BEAS-2B 支气管上皮细胞损伤中的保护作用。我们发现骨化三醇/VDR 系统减少了 PM2.5 处理细胞中 ROS 的形成并恢复了线粒体生物能量学。这种改善与 HIF-1α 核转位减少以及 PGC-1α 蛋白和线粒体基因表达增加相关。这项研究首次表明靶向骨化三醇/VDR 系统可能是一种很有前途的药理学策略，通过促进线粒体生物能量学和调节 PGC-1α 和 HIF-1α 信号传导来减轻 PM2.5 诱导的肺上皮损伤。