Importance of hyaluronan-rich extracellular matrix for haematopoiesis, inflammation and structural remodelling in aortic aneurysms (B08)

在Apoe-/-/ HAS3 -/-小鼠血管破裂减少的血管紧张素ii诱导的腹主动脉瘤和夹层（AAA/AAD）模型中，透明质酸合酶3 （HAS3）基因缺失可提高生存率。此外，在没有HAS3的情况下，没有检测到胸主动脉瘤（TAA），这一观察结果表明，在主动脉解剖过程中，潜在的ha相关病理机制存在部位特异性差异。我们假设沿主动脉对不同应激源的局部区域反应是由特定部位的ha -富基质驱动的，从而确定了TAA和AAA/AAD发生和进展的异质性。

Genetic deletion of hyaluronan synthase 3 (HAS3) improves survival in a model of Angiotensin II-induced abdominal aortic aneurysms and dissections (AAA/AAD) due to reduced vessel ruptures in Apoe-/-/Has3-/- mice. Besides, no thoracic aortic aneurysms (TAA) were detected in the absence of HAS3 – an observation which indicates site-specific differences in the underlying HA-related pathomechanisms along the anatomical course of the aorta. We hypothesise that locoregional responses to distinct stressors along the aorta are driven by the site-specific HA-rich matrix, thereby determining the heterogeneity in the development and progression of TAA and AAA/AAD.