人类骨肌功能障碍中与年龄相关的阿迪波涅丁耐药性:体内和体外证据
Surina Surina1, Lucia Scisciola1, Manuela Giovanna Basilicata1
1Department of Advanced Medical and Surgical Science, University of Campania "Luigi Vanvitelli", Napoli, Italy.
Journal of translational medicine
|March 5, 2026
概括
在衰老过程中阿迪波涅丁的升高反映了细胞的压力和抵抗,而不是有益的信号,有助于萨尔科佩尼亚. 这种与年龄相关的转变涉及AdipoR2下调和骨肌肉中的代谢功能障碍.
科学领域:
- 老年学和肌肉生理学
- 内分泌学和新陈代谢学
背景情况:
- 萨尔科佩尼亚是一种与年龄相关的肌肉质量和功能丧失,矛盾的是,与老年人皮质素升高有关.
- 虽然阿迪波内克通常支持肌肉再生,但其在衰老中的高水平与肌肉健康和性能下降有关.
研究的目的:
- 调查阿迪波涅克丁水平,衰老,身体组成和老年人的身体功能之间的关系.
- 在实验室中探索骨肌细胞中抗子素耐药性的机制.
主要方法:
- 对393名老年人进行了人体测量,身体组成和身体表现的评估.
- 在PBMC中测量了血腺素和AdipoR1/AdipoR2的表达.
- 暴露人类骨肌细胞 (SkMCs) 在体外对阿迪波R激动剂进行细胞反应分析.
主要成果:
- 血腺素与老年人BMI,肌肉质量,肌肉质量和体力表现负相关.
- 在调整身体成分后,阿迪波涅克水平与年龄呈正相关性.
- 阿迪波R2表达与年龄和阿迪波涅克丁水平相反相关,表明阿迪波涅克丁耐药性.
- 在体外,高剂量的AdipoR激动剂诱导了氧化应激,蛋白质稳定性受损,脂质代谢失调,细胞活力降低.
结论:
- 衰老会改变阿迪波内克丁的信号传递,而阿迪波R2的下调会促进系统性抵抗.
- 损坏的AdipoR2功能和过度的AMPK活性导致骨肌肉的氧化还原失衡和代谢功能障碍.
- 这些因素创造了一个"衰老样"的表型,加剧了衰老中的肌肉功能障碍.
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