硫化减轻了血管光滑肌细胞中铁诱导的线粒体功能障碍
Hassan Mustafa Arif1, Ming Fu2, Rui Wang2
1Department of Biology, York University, Toronto, ON, M3J 1P3, Canada.
Biochemical and biophysical research communications
|July 3, 2025
概括
铁过载会损害缺乏囊氨酸γ-酶 (CSE-KO) 的细胞中的线粒体功能. 硫化 (H2S) 处理保护了这些细胞,恢复了线粒体呼吸和膜潜力,突出了H2S.
科学领域:
- 细胞生物学 细胞生物学
- 生物化学 生物化学
- 生理学 生理学 生理学
背景情况:
- 线粒体功能障碍导致细胞压力和疾病.
- 铁过载和氧化应激加重了线粒体损伤.
- 野生型 (WT) 血管光滑肌细胞 (VSMC) 比CSE-KO细胞更好地处理铁.
研究的目的:
- 为了研究铁对CSE-KO VSMCs线粒体呼吸的影响.
- 为了确定硫化 (H2S) 是否可以防止铁引起的线粒体损伤.
主要方法:
- 海马XF96分析以评估线粒体呼吸.
- JC-1染色用于评估线粒体膜潜力.
- 铁暴露下的WT和CSE-KOVSMC之间的比较,有和没有H2S处理.
主要成果:
- 在CSE-KO细胞中,暴露于铁会损害线粒体呼吸 (最大和备用容量).
- WT细胞保持了更高的备用呼吸能力,表明内源的H2S保护.
- 在CSE-KO细胞中,铁诱导的线粒体功能障碍和膜脱极化被H2S治疗逆转.
结论:
- 内源硫化 (H2S) 在VSMC中起着保护性作用,防止铁引起的线粒体功能障碍.
- 在铁过载的CSE-KO细胞中,H2S治疗可以恢复线粒体功能和膜完整性.
- 了解铁-H2S相互作用为缓解铁诱导的细胞损伤提供了治疗潜力.
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