Ascending thoracic aortic aneurysm (ATAA) remains a significant medical concern, with its asymptomatic nature posing diagnostic and monitoring challenges, thereby increasing the risk of aortic wall dissection and rupture. Current management of aortic repair relies on an aortic diameter threshold. However, this approach underestimates the complexity of aortic wall disease due to important knowledge gaps in understanding its underlying pathologic mechanisms.

Since traditional risk factors cannot explain the initiation and progression of ATAA leading to dissection, local vascular factors such as extracellular matrix (ECM) and vascular smooth muscle cells (VSMCs) might harbor targets for early diagnosis and intervention. Derived from diverse embryonic lineages, VSMCs exhibit varied responses to genetic abnormalities that regulate their contractility. The transition of VSMCs into different phenotypes is an adaptive response to stress stimuli such as hemodynamic changes resulting from cardiovascular disease, aging, lifestyle, and genetic predisposition. Upon longer exposure to stress stimuli, VSMC phenotypic switching can instigate pathologic remodeling that contributes to the pathogenesis of ATAA.

This review aims to illuminate the current understanding of cellular and molecular characteristics associated with ATAA and dissection, emphasizing the need for a more nuanced comprehension of the impaired ECM–VSMC network.

升胸主动脉瘤 （ATAA） 仍然是一个重大的医学问题，其无症状性质带来了诊断和监测挑战，从而增加了主动脉壁夹层和破裂的风险。目前主动脉修复术的管理依赖于主动脉直径阈值。然而，由于在理解其潜在病理机制方面存在重要的知识空白，这种方法低估了主动脉壁疾病的复杂性。

由于传统的危险因素无法解释导致夹层的 ATAA 的发生和进展，因此细胞外基质 （ECM） 和血管平滑肌细胞 （VSMC） 等局部血管因子可能隐藏着早期诊断和干预的目标。VSMC 源自不同的胚胎谱系，对调节其收缩力的遗传异常表现出不同的反应。VSMC 向不同表型的转变是对压力刺激的适应性反应，例如由心血管疾病、衰老、生活方式和遗传易感性引起的血流动力学变化。在长时间暴露于应激刺激下时，VSMC 表型转换可引发病理重塑，从而导致 ATAA 的发病机制。

本综述旨在阐明当前对与 ATAA 和解剖相关的细胞和分子特征的理解，强调需要对受损的 ECM-VSMC 网络进行更细致的理解。