In this study, we carried out a clinical sample study, and and studies to evaluate the effect of SIRT6 and SIRT6-mediated vascular smooth muscle senescence on the development of abdominal aortic aneurysm (AAA). AAA specimen showed an increased P16, P21 level and a decreased SIRT6 level compared with control aorta. Time curve study of Ang II infusion AAA model showed similar P16, P21 and SIRT6 changes at the early phase of AAA induction. The overexpression of SIRT6 significantly prevented AAA formation in Ang II infusion model. The expression of P16 and P21 was significantly reduced after SIRT6 overexpression. SIRT6 overexpression also attenuated chronic inflammation and neo-angiogenesis in Ang II infusion model. The overexpression of SIRT6 could attenuate premature senescence, inflammatory response and neo-angiogenesis in human aortic smooth muscle cells (HASMC) under Ang II stimulation. SIRT6 overexpression could limit AAA formation via attenuation of vascular smooth muscle senescence, chronic inflammation and neovascularity.

中文翻译：

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SIRT6介导的血管平滑肌细胞衰老参与腹主动脉瘤的发病机制

在本研究中，我们开展了临床样本研究，并研究评估SIRT6和SIRT6介导的血管平滑肌衰老对腹主动脉瘤（AAA）发展的影响。与对照主动脉相比，AAA 标本显示 P16、P21 水平升高，SIRT6 水平降低。 Ang II输注AAA模型的时间曲线研究显示在AAA诱导早期相似的P16、P21和SIRT6变化。 SIRT6 的过度表达显着阻止 Ang II 输注模型中 AAA 的形成。 SIRT6过表达后P16和P21的表达显着降低。 SIRT6 过表达还可以减轻 Ang II 输注模型中的慢性炎症和新血管生成。 SIRT6 的过表达可以减弱 Ang II 刺激下人主动脉平滑肌细胞 (HASMC) 的过早衰老、炎症反应和新血管生成。 SIRT6 过度表达可以通过减弱血管平滑肌衰老、慢性炎症和新血管形成来限制 AAA 形成。