缺陷的蛋白质固硫化与肥胖相关的骨肌肉功能障碍有关:SIRT-1的作用
M Smimmo1, V Casale1, D D'Andrea2
1Department of Pharmacy, School of Medicine and Surgery, University of Naples Federico II, Naples, Italy.
Redox biology
|May 3, 2025
概括
减少的MPST衍生硫化 (H2S) 信号损害了肥胖患者的骨肌功能. 补充H2S可以提高肌肉性能并恢复蛋白质固硫化,提供潜在的治疗点.
科学领域:
- 生物化学 生物化学
- 生理学 生理学 生理学
- 代谢疾病 代谢疾病
背景情况:
- 骨肌肉 (SKM) 中因肥胖引起的宫外脂肪会损害肌肉质量和性能.
- 将肥胖与SKM功能障碍联系在一起的精确分子机制尚未完全理解.
研究的目的:
- 调查MPST衍生硫化 (H2S) 信号在与肥胖相关的SKM功能障碍中的作用.
- 探索H2S作为一种潜在的治疗干预措施,以改善肥胖症中的SKM健康.
主要方法:
- 使用肥胖的db/db小鼠和Mpst淘汰赛 (Mpst-/-) 小鼠模型.
- 评估了MPST表达,蛋白质持续硫化和肌肉性能.
- 在体内和体外使用肌管模型补充H2S.
- 分析了来自肥胖个体的人类肌肉活检.
主要成果:
- 肥胖小鼠和肌管显示MPST表达和蛋白质化减少,与肌肉功能受损相关.
- 补充H2S改善了运动运动活动,并恢复了蛋白质固硫化,包括SIRT-1.
- 在肥胖个体的肌肉活检中观察到减少MPST表达.
结论:
- 受损的MPST衍生的H2S信号是导致肥胖相关的SKM功能障碍的关键因素.
- 通过SIRT-1持续硫化,MPST/H2S通路对于保持SKM健康至关重要.
- 准H2S通路为与肥胖相关的肌肉损伤提供了一个有希望的治疗策略.
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