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性饮食诱导多个器官中的p53依赖的细胞衰老
Sung-Jen Wei1,2, Joseph R Schell1,2, E Sandra Chocron1,2
1Department of Radiation Oncology, Mays Cancer Center at UT Health San Antonio MD Anderson, Joe R. and Teresa Lozano Long School of Medicine, San Antonio, TX, USA.
Science advances
|May 17, 2024
概括
性饮食 (KD) 可以诱导细胞衰老,衰老细胞的状态,在像心脏和脏这样的器官. 这种效应是可逆的老化剂或间歇性KD方法.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 生理学 生理学 生理学
背景情况:
- 性饮食 (KD) 是高脂肪,低碳水化合物饮食,以减肥和改善某些健康状况而闻名.
- 然而,性饮食的潜在有害影响需要进一步调查.
- 细胞衰老,一种不可逆转的细胞循环停止状态,与衰老和与年龄相关的疾病有关.
研究的目的:
- 研究基因饮食对多个器官细胞衰老的影响.
- 为了阐明基底的分子机制KD诱导的衰老.
- 探索缓解KD相关衰老的潜在干预措施.
主要方法:
- 在不同的年龄段,小鼠被食两种不同的代饮食.
- 分析包括评估器官中的细胞衰老标志物,利用淘汰小鼠 (p53,caspase-2) 和使用特定抑制剂 (AMPK,p21,caspase-2).
- 衰老相关分泌表型 (SASP) 生物标志物被测量在小鼠血清和人类患者血中,来自KD临床试验.
主要成果:
- 性饮食诱导了小鼠的心脏和脏中的细胞衰老.
- 这种效应是由腺单酸盐激活蛋白激酶 (AMPK) 途径介导的,鼠标双分钟2 (MDM2) 的caspase-2失活,导致p53积累和p21诱导.
- 在基饮食的小鼠和人类中观察到 SASP 生物标志物升高,这在老化药物或间歇性 KD 中是可逆的.
结论:
- 性饮食可以通过特定的分子通路促进细胞衰老.
- 间歇性KD和老化疗法显示出预防或逆转KD诱导的衰老的潜力.
- 这些发现强调了性饮食的情境影响,强调了个性化方法的必要性.
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