Stanford type A aortic dissection (TAAD) is one of the most dangerous diseases of acute aortic syndrome. Molecular pathological studies on TAAD can aid in understanding the disease comprehensively and can provide insights into new diagnostic markers and potential therapeutic targets. In this study, we defined the molecular pathology of TAAD by performing transcriptome sequencing of human ascending aortic tissues. Pathway analysis revealed that activated inflammation, cell death and smooth muscle cell degeneration are the main pathological changes in aortic dissection. However, autophagy is considered to be one of the most important biological processes, regulating inflammatory reactions and degenerative changes. Therefore, we focused on the pathological role of autophagy in aortic dissection and identified 10 autophagy-regulated hub genes, which are all upregulated in TAAD. These results indicate that exaggerated autophagy participates in the pathological process of aortic dissection and may provide new insight for further basic research on TAAD.

中文翻译：

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斯坦福 A 型主动脉夹层中的夸大自噬：人类升主动脉组织的转录组试验分析

斯坦福 A 型主动脉夹层 (TAAD) 是急性主动脉综合征中最危险的疾病之一。对 TAAD 的分子病理学研究可以帮助全面了解疾病，并可以提供对新诊断标志物和潜在治疗靶点的见解。在这项研究中，我们通过对人类升主动脉组织进行转录组测序来定义 TAAD 的分子病理学。通路分析显示，激活的炎症、细胞死亡和平滑肌细胞变性是主动脉夹层的主要病理变化。然而，自噬被认为是最重要的生物过程之一，调节炎症反应和退行性变化。因此，我们关注自噬在主动脉夹层中的病理作用，并确定了 10 个自噬调节的枢纽基因，这些都在 TAAD 中上调。这些结果表明夸大的自噬参与了主动脉夹层的病理过程，可能为进一步的 TAAD 基础研究提供新的见解。