Supplementary Tables

This study reveals the pivotal role of GR-mediated transcriptional regulation in stress-induced FLS in chickens. Chronic stress modeled with CORT disrupted mitochondrial SC assembly, impairing electron transport, elevated ROS production, and liver steatosis. Notably, the downregulation of Complex I assembly factors (NDUFAF5, NDUFAF7, and TIMMDC1) and reduced GR binding to NDUFAF5 were key mechanisms. These findings provide new insights into stress-driven mitochondrial dysfunction in broiler FLS.

本研究揭示了糖皮质激素受体（glucocorticoid receptor, GR）介导的转录调控在鸡应激诱导的脂肪肝综合征（Fatty Liver Syndrome, FLS）中的关键作用。以皮质酮（corticosterone, CORT）构建的慢性应激模型可破坏线粒体超复合物组装，损伤电子传递过程，提升活性氧（reactive oxygen species, ROS）生成水平，并引发肝脂肪变性。值得注意的是，复合物I组装因子（NDUFAF5、NDUFAF7与TIMMDC1）的表达下调，以及GR与NDUFAF5的结合能力减弱，是该病理过程的核心机制。上述研究结果为肉鸡应激诱导线粒体功能障碍的脂肪肝综合征提供了全新的研究视角。