UFMylation维持YAP的稳定性,以促进血管内皮细胞衰老
Yanan Liu1,2, Min Zuo2, Aiwei Wu2
1Department of Geriatric Medicine, Center of Coronary Circulation, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
iScience
|February 24, 2025
概括
细胞衰老驱动血管衰老和心血管疾病. 这项研究揭示了UFMylation稳定YAP,促进衰老,并确定UFMylation抑制作为潜在的抗衰老疗法.
科学领域:
- 心血管生物学 心血管生物学
- 细胞衰老 细胞衰老
- 分子机制的分子机制
背景情况:
- 内皮细胞 (EC) 衰老有助于血管衰老和心血管疾病 (CVD).
- 海马-Yes相关蛋白 (YAP) 信号通路与衰老相关的心血管疾病有关.
研究的目的:
- 研究YAP和UFMylation在内皮细胞衰老中的作用.
- 探索UFMylation作为血管衰老的潜在治疗点.
主要方法:
- 在人静脉内皮细胞 (HUVECs) 中评估了YAP水平和衰老.
- 研究了抑制UFMylation对衰老细胞和老年小鼠的影响.
- 在老化EC中检查了UFM1-修改的YAP.
主要成果:
- 在衰老的HUVEC中,YAP升高,YAP抑制降低了衰老.
- 在衰老细胞中,UFMylation活动和YAP水平都增加了.
- 在老化的EC中,UFM1修改后的YAP增强了YAP的稳定性.
- 化合物8.5,一种UFMylation抑制剂,在老年小鼠中缓解了血管衰老.
结论:
- UFMylation稳定了YAP,促进了内皮细胞衰老和血管衰老.
- 准UFMylation为抗衰老干预提供了一个新的治疗策略.
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