| 摘要: |
| 急性主动脉夹层(AAD)是由主动脉壁中层撕裂所致的急症,往往高度致命。目前对于遗传性AAD的发病机制了解较多,但非遗传性AAD的发病机制仍不明确。肌腱蛋白-C(TnC)为细胞外基质(ECM)中的一种六聚体糖蛋白,有多项研究表明组织受机械压力刺激时其表达上调。TnC基因敲除(TnC-KO)小鼠主动脉内压力明显上升并易发生AAD。与野生型(WT)小鼠相比,发生AAD的TnC-KO鼠主动脉壁内炎症细胞显著增多且炎症反应加强。TnC可能通过调整ECM结构、调节血管平滑肌细胞(VSMC)功能以及抑制炎症反应来保护主动脉使其免于AAD。本文综述TnC在AAD发生发展过程中的作用。 |
| 关键词: 腱糖蛋白-C 主动脉瘤 动脉瘤 机械压力 基因敲除 |
| DOI：10.3724/SP.J.1008.2015.1238 |
| 投稿时间：2015-03-30修订日期：2015-05-13 |
| 基金项目: |
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| Research progress of tenascin-C in acute aortic dissection |
| AN Zhao,XU Zhi-yun* |
(Department of Cardiothoracic Surgery, Changhai Hospital, Second Military Medical University, Shanghai 200433, China
*Corresponding author.) |
| Abstract: |
| Acute aortic dissection(AAD) is a medical emergency caused by the destruction of the aortic tunica media and is always fatal. Genetic disorders are known to be responsible for AAD, but little is known about the etiology of other non-genetic cases. Tenascin-C(TnC) is a large extracellular matrix glycoprotein and mechanical stretching can up-regulate TnC expression. TnC knockout (TnC-KO) mice have higher blood pressure in the aortic artery and are liable to develop AAD; and mice with AAD have more inflammatory cells in the aortic tissue. TnC prevents aorta from AAD by regulating ECM structure, regulating vascular smooth muscle cell function and inhibiting inflammatory response in the aorta. In this paper we reviewed the role of TnC in the development and progression of AAD. |
| Key words: tenascin-c aortic aneurysm dissecting aneurysm mechanical stretch gene knockout |
