ER蛋白质毒性压力驱动热应激肠道上皮细胞中的线粒体功能障碍
Shuai Gao1,2, Xiaocong Zheng3, Yi Jiang1
1Hainan Laboratory Animal Research Center, Sanya Institute of Hainan Academy of Agricultural Sciences, Sanya 572000, China.
Cells
|March 14, 2026
概括
热应激通过破坏细胞能量生产,损害牲畜肠道. 向内质网膜 (ER) 压力提供了一种潜在的解决方案,可以保护肠道细胞,并在热浪期间改善牲畜健康.
科学领域:
- 动物科学动物科学
- 细胞生物学 细胞生物学
- 环境科学 环境科学
背景情况:
- 气候变化加剧了热浪,威胁到畜牧业的生产.
- 热应激会破坏肠道屏障的完整性,导致细胞损伤.
- 细胞内膜网膜 (ER) 应激和线粒体功能障碍是热应激的已知的细胞后果.
研究的目的:
- 为了研究ER压力和线粒体功能障碍之间的因果关系在热应激肠细胞中.
- 阐明动物热应激诱导的肠损伤背后的分子机制.
- 探索针对ER压力的治疗策略,以减轻热应激效应.
主要方法:
- 在猪肠上皮细胞 (IPEC-J2) 中利用了综合转录组,代谢组和功能分析.
- 在急性热应激下评估线粒体生物能学和细胞超结构.
- 使用药理抑制和诱导ER压力来验证发现.
主要成果:
- 热应激诱导了显著的转录和代谢重编程,包括ER应激激活.
- 线粒体生物能学严重受损,呼吸和ATP产生减少.
- 药理上抑制ER压力减弱了线粒体功能障碍和细胞损伤.
结论:
- 热应激诱导的ER压力关键介导线粒体功能障碍和肠细胞中的肠损伤.
- 针对ER压力是一个有希望的治疗策略,以减轻牲畜中热应激引起的肠损伤.
- 了解这些细胞机制对于在气候变化下保持牲畜健康和生产力至关重要.
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