老化的微生物群通过PPARα/PGC1α通路加剧心力衰竭
Han Xu1, Ouyang Li1, Dayoung Kim1
1Department of Gerontology, Huadong Hospital Affiliated to Fudan University, Shanghai, China; Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai, China.
概括
来自老年捐赠者的便微生物群移植通过改变肠道细菌和损害心脏功能,使小鼠的心脏衰竭恶化. 激活PPARα/PGC1α通路可以逆转这些负面影响.
科学领域:
- 微生物学 微生物学
- 心脏病学 心脏病学
- 老年学是一门学科.
背景情况:
- 肠道微生物群失调与衰老和各种疾病有关.
- 老化肠道微生物群在心力衰竭 (HF) 中的具体作用尚不清楚.
研究的目的:
- 研究来自老年捐赠者的体微生物群移植 (FMT) 对心力衰竭进展的影响.
- 阐明潜在的机制,重点关注代谢变化和信号通路.
主要方法:
- 从老年捐赠者的便微生物群移植 (FMT) 给HF小鼠.
- 评估心脏功能,身体活动,代谢参数和心脏组织学.
- 对PPARα/PGC1α信号通路的分析.
主要成果:
- 在老年FMT改变了肠道微生物群的组成和心脏功能和身体活动受损的HF小鼠.
- 老年FMT诱导的代谢功能障碍,包括体重增加,葡萄糖耐受性受损和脂肪积累增加.
- 年龄化的FMT导致心上脂肪积累,心肌细胞缩,纤维化,亡,并抑制了PPARα/PGC1α信号传递.
结论:
- 老化肠道微生物群通过代谢失调和心脏损伤加剧心力衰竭.
- PPARα/PGC1α信号通路是老年FMT诱导心力衰竭的关键调解者.
- 激活PPARα可以改善老年FMT对新陈代谢和心脏健康的不良影响.
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