摘要
胸主动脉瘤(TAA)是累及主动脉壁的致命性疾病。目前,TAA的发病机制尚不完全清楚,可能存在遗传及环境因素的共同作用,同时通过血流动力学变化、透壁炎症反应及细胞外基质降解和重构等机制,引起动脉弹性和胶原蛋白破坏,导致主动脉壁变薄并向外膨胀及动脉瘤形成。本文综述TAA分子发病机制的研究进展。
出处
《国际心血管病杂志》
2008年第5期297-300,共4页
International Journal of Cardiovascular Disease
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