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慢性酒精消费加剧与缺血相关的骨肌线粒体功能障碍在外周动脉疾病的小鼠模型中

Emma Fletcher¹, Dimitrios Miserlis², Evlampia Papoutsi¹

¹Department of Public Health, Usha Kundu MD College of Health, University of West Florida, Pensacola, FL, USA.

Biochimica et biophysica acta. Molecular basis of disease

|November 24, 2024

概括

高脂肪,高酒精饮食会通过损害线粒体来加剧外周动脉疾病 (PAD) 的肌肉损伤. 降低脱酶2 (ALDH2) 与这种功能障碍有关,这表明它是治疗点.

科学领域:

线粒体生物学线粒体生物学
血管疾病研究研究.
营养科学营养科学

背景情况:

周围动脉疾病 (PAD) 会导致肌肉损伤,增加残疾和死亡率.
酒精和高脂肪饮食对PAD相关的肌肉疾病 (肌肉病) 的综合影响尚不清楚.
线粒体功能障碍是PAD肌病的关键因素.

研究的目的:

为了研究慢性酒精和高脂肪饮食如何影响肌肉氧化应激和线粒体健康在PAD的小鼠模型.
探索阿尔代脱酶2 (ALDH2) 水平,氧化应激和PAD中的线粒体功能障碍之间的关系.
确定高脂肪糖 (HFS) 饮食和乙醇 (EtOH) 消费对PAD肌病的综合影响.

主要方法:

通过关动脉绑定建立了外周动脉疾病 (PAD) 的小鼠模型.
给小鼠提供高脂肪糖 (HFS) 或低脂肪糖 (LFS) 饮食,并暴露在乙醇 (EtOH) 或水中.
分析了肌肉组织的氧化应激,线粒体含量,功能和质量控制,重点是ALDH2.

主要成果:

同时高脂肪糖 (HFS) 饮食和乙醇 (EtOH) 食在PAD小鼠中加剧了缺血性肌肉线粒体病变.
肌肉内阿尔德海德脱酶2 (ALDH2) 水平在HFS + EtOH小鼠的缺血肢体下降.
减少的ALDH2与增加的氧化应激和线粒体功能障碍标志物有很强的相关性.

结论:

化脱酶2 (ALDH2) 在缓解PAD中线粒体功能障碍方面发挥着至关重要的作用.
向ALDH2可能为改善PAD患者肌肉线粒体功能提供治疗策略,特别是那些酒精和脂肪摄入量高的人.
饮食干预与潜在的基于ALDH2的疗法相结合,可能有利于PAD管理.

关键词:

阿尔德脱酶-2 的作用.长期的酒精和脂肪消费.后肢缺血后肢缺血是什么肌肉内线粒体功能障碍肌肉内线粒体功能障碍氧化应激是一种氧化应激.周围动脉疾病是什么?

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