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通过CX43-PARP1轴,NAD+可通过CX43-PARP1轴拯救因衰老引起的血脑屏障损伤

Rui Zhan¹, Xia Meng², Dongping Tian³

¹The Institute of Cardiovascular Sciences, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Beijing Key Laboratory of Cardiovascular Receptors Research, Health Science Center, Peking University, Beijing 100191, China; Research Center for Cardiopulmonary Rehabilitation, University of Health and Rehabilitation Sciences Qingdao Hospital (Qingdao Municipal Hospital), School of Health and Life Sciences, University of Health and Rehabilitation Sciences, Qingdao 266071, China.

|September 8, 2023

概括

衰老会损害血脑屏障 (BBB),因为减少了连接素43 (CX43). 用PARP1抑制剂或NMN恢复这种途径可以防止BBB泄漏并保护大脑.

科学领域:

神经科学是一个神经科学.
血管生物学血管生物学
衰老研究研究衰老研究

背景情况:

血脑屏障 (BBB) 功能障碍是衰老的标志,与认知衰退和神经退行有关.
驱动与年龄相关的BBB泄漏的特定分子机制和潜在的预防策略仍然在很大程度上是未知的.

研究的目的:

为了研究联结素43 (CX43) 在与年龄相关的BBB功能障碍中的作用.
确定治疗目标,以防止老化过程中的BBB泄漏.

主要方法:

在老年小鼠中单核转录组学,以确定大脑血管细胞的变化.
在小鼠中遗传删除CX43以评估其对BBB功能的影响.
药理上抑制了多PADP-ribose) 聚合酶1 (PARP1) 和尼古丁胺胺 mononucleotide (NMN) 的补充.

主要成果:

在老年小鼠和人类大脑样本中观察到CX43表达的减少.
CX43缺乏症加剧了与年龄相关的BBB泄漏,独立于其间隙连接功能.
CX43通过SIRT3途径调节NAD+水平和线粒体功能,并对PARP1活动产生负面影响.
抑制PARP1或补充NMN可以恢复NAD+水平并改善BBB泄漏.

结论:

内皮CX43-PARP1-NAD+通路对于在衰老期间保持BBB完整性至关重要.
针对这种途径提供了一个潜在的治疗策略,以打击与年龄相关的BBB泄漏和神经退行.

关键词:

这是BBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBBB 在CX43CX43CX43CX43CX43CX43 这是NAD (((+)PARP1 的第一部分老化的老化衰老的老化长期使用NMN进行NMN管理.

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