列宁血管酶系统诱导的肌肉衰竭:假定机制和临床医生的影响
Baris Afsar1,2, Rengin Elsurer Afsar3,4, Yasar Caliskan4
1Department of Nephrology, School of Medicine, Suleyman Demirel University, Isparta, Turkey. afsarbrs@yahoo.com.
Molecular and cellular biochemistry
|May 29, 2024
概括
氨素系统 (RAS) 影响肌肉消耗. 它的经典途径,通过 ангиотензинII (AngII),促进肌肉损失,而非经典途径,通过 ангиотензин1-7提供保护.
科学领域:
- 生理学 生理学 生理学
- 分子生物学分子生物学
- 老年学是一门学科.
背景情况:
- 氨酶系统 (RAS) 在调节生理过程中起着至关重要的作用.
- RAS的失调与各种病理状况有关,包括肌肉衰竭和肉症.
- RAS包括不同的古典和非古典路径,对骨肌有相反的影响.
研究的目的:
- 审查经典和非经典RAS途径影响肌肉消耗的多方面的机制.
- 探索针对RAS用于治疗肉症的潜在临床影响.
- 确定知识差距,并建议未来的研究方向在RAS介导的肌肉缩.
主要方法:
- 对研究Renin Angiotensin系统及其组成部分的研究进行文献综述.
- 对RAS诱导的肌肉衰竭背后的分子和细胞机制的分析.
- 关于非经典RAS通路的保护作用的证据综合.
主要成果:
- 通过 ангиотензинII (AngII) 和AT1受体介导的经典RAS途径,通过减少食物摄入,增加蛋白质解离,亡,炎症,氧化应激和线粒体功能受损,促进肌肉消耗.
- 非经典的RAS通路,涉及 ангиотензин 1-7 和Mas受体,可以抵消这些代谢效应,从而提供对萨尔科佩尼亚的保护.
- 具体的分子标包括素,神经Y,IGF-1,mTOR,FOXO,酶,TNF-α和IL-6.
结论:
- 经典和非经典RAS通路之间的平衡对于维持骨肌肉质量和功能至关重要.
- 准RAS的特定组件是一个有希望的治疗策略,用于对抗肌肉衰竭和肉症.
- 需要进一步的研究,以充分阐明RAS及其临床应用中的复杂相互作用.
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