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首页> 外文期刊>Journal of atherosclerosis and thrombosis. >Crossing Bridges between Extra- and Intra-Cellular Events in Thoracic Aortic Aneurysms
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Crossing Bridges between Extra- and Intra-Cellular Events in Thoracic Aortic Aneurysms

机译：胸主动脉瘤细胞外和细胞内事件之间的桥梁

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Thoracic aortic aneurysms (TAAs) are common, life-threatening diseases and are a major cause of mortality and morbidity. Over the past decade, genetic approaches have revealed that 1) activation of the transforming growth factor beta (TGF-β) signaling, 2) alterations in the contractile apparatus of vascular smooth muscle cells (SMCs), and 3) defects in the extracellular matrix (ECM) were responsible for development of TAAs. Most recently, a fourth mechanism has been proposed in that dysfunction of mechanosensing in the aortic wall in response to hemodynamic stress may be a key driver of TAAs. Interestingly, the elastin-contractile unit, which is an anatomical and functional unit connecting extracellular elastic laminae to the intracellular SMC contractile filaments, via cell surface receptors, has been shown to play a critical role in the mechanosensing of SMCs, and many genes identified in TAAs encode for proteins along this continuum. However, it is still debated whether these four pathways converge into a common pathway. Currently, an effective therapeutic strategy based on the underlying mechanism of each type of TAAs has not been established. In this review, we will update the present knowledge on the molecular mechanism of TAAs with a focus on the signaling pathways potentially involved in the initiation of TAAs. Finally, we will evaluate current therapeutic strategies for TAAs and propose new directions for future treatment of TAAs.
机译：胸主动脉瘤（TAA）是常见的威胁生命的疾病，并且是死亡率和发病率的主要原因。在过去的十年中，遗传方法揭示了1）激活转化生长因子β（TGF-β）信号转导，2）血管平滑肌细胞（SMC）收缩装置的改变，以及3）细胞外基质中的缺陷（ECM）负责TAA的开发。最近，已经提出了第四种机制，即主动脉壁的机械传感功能失调可能是TAA的主要驱动力，而该功能失调可能是血液动力学应力的响应。有趣的是，弹性蛋白收缩单元是一种通过细胞表面受体将细胞外弹性薄片连接到细胞内SMC收缩细丝的解剖学和功能单元，已显示在SMC的机械传感中起着关键作用，并且许多基因在TAA沿该连续体编码蛋白质。但是，这四个途径是否会融合成一个共同的途径仍存在争议。目前，尚未建立基于每种TAA潜在机制的有效治疗策略。在这篇综述中，我们将更新有关TAA分子机制的现有知识，重点是可能涉及TAA起始的信号通路。最后，我们将评估TAA的当前治疗策略，并为TAA的未来治疗提出新的方向。

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