Orai1通过调节光滑肌肉细胞表型转换,参与高血压引起的冠状动脉功能障碍
Hao Wang1, Mei-Ying Liang2,3, Yong-Jiang Cai2,3
1Department of Cardiology, the Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
概括
高血压通过调节Orai1来损害冠状动脉,这是一种对储存运行入 (SOCE) 至关重要的蛋白质. 这一途径驱动血管光滑肌肉细胞的转化,有助于高血压引起的冠状动脉功能障碍.
科学领域:
- 心血管生物学 心血管生物学
- 分子医学是分子医学.
- 高血压研究 高血压研究
背景情况:
- 高血压是血管改造和动脉样硬化的主要危险因素.
- 由STIM/Orai1蛋白质介导的储存运行的入 (SOCE) 与心血管病理有关.
- 在高血压引起的冠状动脉功能障碍中,Orai1介导的SOCE的确切作用尚未完全理解.
研究的目的:
- 研究Orai1/NFAT/calcineurin信号通路在高血压引起的冠状动脉血管收缩障碍中的作用.
- 阐明高血压影响冠状动脉光滑肌细胞 (CASMCs) 的机制.
主要方法:
- 使用自发高血压大鼠 (SHRs) 和Wistar大鼠.
- 暴露在高水静压 (180 mmHg) 的CASMC中.
- 评估了冠状动脉收缩,SOCE抑制,以及STIM1,Orai1,Calcineurin-NFAT2,OPN和SMMHC的表达.
主要成果:
- 与Wistar大鼠相比,SHRs中激素诱导的冠状动脉收缩减少了.
- 高血压/高血压增加了STIM1/Orai1,Calcineurin-NFAT2和OPN的表达,同时降低了CASMC中的SMMHC.
- 干预的目标是Orai1/SOCE调节的STIM1,氨酸-NFAT2和表型标记物.
结论:
- 高血压通过Orai1上调来诱导冠状动脉血管功能障碍.
- Orai1对于通过氨酸-NFAT通路进行血管光滑肌细胞的表型转化至关重要.
- 针对Orai1/Calcineurin-NFAT通路可能为与高血压相关的冠状动脉功能障碍提供治疗策略.
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