通过激活ZBP1-介导的亡,TMAO诱导了衰老
1Department of Clinical Diagnostics, Hebei Medical University, Shijiazhuang, 050017, China. 18201400@hebmu.edu.cn; Department of Pharmacy, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, Pudong, Shanghai, China. mafenfen2005@126.com.
Physiological research
|March 11, 2026
概括
三甲基胺-N-氧化物 (TMAO) 通过激活ZBP1介导的亡,加速衰老. 抑制TMAO形成可能为与年龄相关的衰退提供潜在的治疗策略.
科学领域:
- 老年学和科:研究衰老的分子机制.
背景情况:
- 衰老与增加的功能障碍有关,其特点是肌素和血尿素的升高.
- 三甲基胺-N-氧化物 (TMAO) 水平在老年脏中升高,这表明它可能在衰老过程中发挥作用.
研究的目的:
- 通过激活亡,确定TMAO是否有助于脏衰老.
- 探索抑制TMAO形成的潜力,作为治疗衰老的治疗干预措施.
主要方法:
- 在年轻 (3个月大) 和老 (18个月大) 雄性C57BL/6J小鼠中,对功能,纤维化,TMAO水平和衰老标志物的比较.
- 在小鼠体内注射TMAO以评估其对脏衰老标志物的直接影响.
- 用DMB治疗,这是TMAO形成的抑制剂,以评估其保护作用.
主要成果:
- 与年轻对照组相比,老老鼠的血肌素,血尿酸,纤维化,血TMAO和衰老标志物显著增加.
- TMAO的使用诱导了功能障碍标志物,纤维化,衰老和亡途径激活 (ZBP1,RIPK3,MLKL) 的时间依赖性增加.
- DMB治疗显著改善了功能障碍,减少了衰老标志物,改善了纤维化,表明了TMAO的有害作用.
结论:
- 通过激活ZBP1介导的亡,TMAO诱导脏衰老.
- 抑制TMAO生成为缓解脏衰老提供了一个有希望的治疗途径.
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