在心力衰竭期间,在缩肌肉中减少了去除反应性化物的代谢途径
Mamata Chaudhari1, Igor Zelko1, Pawel Lorkiewicz1
1University of Louisville.
Research square
|December 4, 2023
概括
心力衰竭导致肌肉衰竭,因为它减少了有毒的化物的去除和保护性化合物的合成,如肉素. 骨肌肉中的这些代谢变化有助于缩.
科学领域:
- 生物化学 生物化学
- 生理学 生理学 生理学
- 病理学 病理学 病理学
背景情况:
- 氧化应激和有毒的脂质过氧化产品 (例如,HNE,acrolein) 导致心力衰竭的肌肉损耗.
- 骨肌肉通常通过酶和核像肉氨酸这样的核来去除这些化物.
- 在心力衰竭期间,骨肌肉中 aldehyde 排毒和 carnosine 合成的代谢途径尚未研究.
研究的目的:
- 为了研究心力衰竭对涉及化物解毒和骨肌肉中化二合成的代谢途径的影响.
- 在心力衰竭模型中,确定受损路径是否会导致肌肉缩.
主要方法:
- 在小鼠中诱导了一种心力衰竭的跨管收缩 (TAC) 模型.
- 分析了骨肌肉重量,缩和炎症标记物 (Atrogin1,TNF-α) 和化蛋白添加物 (HNE,acrolein).
- 量化了阿尔代代谢酶 (AKR1B1,ALDH2) 和基二 (卡诺辛,安森林) 以及它们的合成/运输蛋白 (CARNS,TAUT) 的水平.
主要成果:
- TAC诱导的心力衰竭导致身体和肌肉重量下降,缩/炎症标志物增加,以及骨肌中的HNE/acrolein adducts升高.
- 阿尔德脱酶2 (ALDH2) 的表达减少,而阿尔多减少酶 (AKR1B1) 则保持不变.
- 肉氨酸和氨酸的水平降低,从而降低了肌肉去除化物的能力.
- 肉氨酸合成酶 (CARNS) 和氨基酸载体TAUT的表达减少.
结论:
- 心力衰竭减少了负责排毒骨肌肉中的脂质过氧化产品的代谢途径.
- 降低合成和水平的histidyl dipeptides,特别是卡诺辛,损害了阿尔德海德的去除能力.
- 骨肌肉中的这些代谢功能障碍可能有助于心力衰竭期间肌肉消耗的发展.
关键词:
一个安塞林.缩性缩 (英语:Atrophy atrophy) 是一种损伤.卡诺西尼 (Carnosine) 是一种类型的肉素.心脏衰竭是因为心脏衰竭.肌肉消耗 肌肉消耗 肌肉消耗乌比奎蛋白质酶体通路更多相关视频
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