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暴露在寒冷中可以通过自性保护中枢动脉化通过自性发展

Fu-Xing-Zi Li¹, Jun-Jie Liu², Feng Xu¹

¹Department of Metabolism and Endocrinology, National Clinical Research Center for Metabolic Disease, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.

Journal of nanobiotechnology

|July 17, 2023

概括

暴露于寒冷的温度会通过增强外体介导自来减缓血管化. 暴露于冷的外体 (CT-Exo) 通过miR-320a-3p保护中枢动脉化 (MAC),激活AMPK/mTOR通路.

科学领域:

心血管生物学心血管生物学
血管医学血管医学
细胞生物学细胞生物学

背景情况:

中枢动脉化 (MAC) 是一种与心血管事件增加相关的全身血管疾病.
环境温度是影响心血管健康的已知因素,但其对MAC的具体影响仍未得到充分研究.
了解MAC的新型治疗途径至关重要,因为它与心血管疾病相关.

研究的目的:

在小鼠模型中研究寒冷温度暴露对中枢动脉化的发展的影响.
阐明潜在的分子机制,特别是外体和微RNAs在调解寒冷暴露的保护作用中的作用.
探索冷暴露外体的潜力,作为预防或治疗MAC的治疗策略.

主要方法:

小鼠被暴露在低温 (CT) 或室温 (RT) 中30天.
从CT和RT小鼠 (CT-Exo和RT-Exo) 中分离出血衍生的外体,并应用于血管光滑肌细胞 (VSMC).
使用了体外和体内血管化的模型,包括维生素D (VD) 诱导的化和β-糖酸盐 (β-GP) 诱导的化.
研究的机制包括自标志物 (AMPK/mTOR通路),微RNA分析 (miR-320a-3p) 和基因分析 (PDCD4).

主要成果:

与室温 (RT) 相比,暴露于寒冷温度 (CT) 在小鼠中显著减缓了维生素D诱导的血管化的形成.
来自暴露于寒冷的小鼠 (CT-Exo) 的外基因组缓解了VSMC中的化和衰老,并通过AMPK/mTOR途径促进了自.
在CT-Exo和CT小鼠胸前大动脉血管中,miR-320a-3p的含量很高;其下调抑制了自和抗化作用.
CT-Exo治疗在体内减少了MAC的形成,这种效应被外体酶抑制剂和miR-320a-3p下调调节部分逆转.

结论:

长时间暴露在寒冷中可能是一个可行的策略,以减轻中枢动脉化的发生和进展.
暴露于冷的外体 (CT-Exo) 对MAC的启动和进展产生保护作用,主要通过miR-320a-3p/PDCD4轴和AMPK/mTOR介导的自途径.
这项研究强调了一种新的外体介导机制,即环境温度影响血管健康,为心血管疾病提供潜在的治疗点.

关键词:

动脉的化动脉的化自自是一种自的过程.暴露于寒冷的情况.在PDCD4中使用PDCD4.由等离子体衍生出来的外体细胞.衰老是一种衰老.在 miR-320a-3p 中.

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