State Key Laboratory of Cardiovascular Disease, Department of Cardiology, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Department of Geriatric Dentistry, National Medical Products Administration Key Laboratory for Dental Materials, National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing Laboratory of Biomedical Materials, Peking University School and Hospital of Stomatology, Beijing, China.
Exp Cell Res. 2024 Oct 1;442(2):114247. doi: 10.1016/j.yexcr.2024.114247. Epub 2024 Sep 12.
Thoracic aortic aneurysm and dissection (TAAD) is a devastating macrovascular disease, and its pathogenic mechanisms have not been well clarified. This study aimed to investigate the role of PANoptosis, which is newly defined programmed cell death (PCD) and characterized by pyroptosis, apoptosis, and necroptosis, in the pathogenesis of TAAD. We found that the expression of initiator factor Z-DNA binding protein 1 (ZBP1) and PANoptosis-related genes were upregulated in the β-aminopropionitrile (BAPN) + Angiotensin II (Ang II)-induced TAAD mice. Ang II stimuli enhanced the expression of ZBP1, promoted the generation of bioactive GSDMD (Gasdermin D) fragments, the cleavage of Caspase 3, and increased the phosphorylation of mixed lineage kinase domain-like pseudokinase (MLKL) in human aortic vascular smooth muscle cells (HASMCs), indicating the activation of hallmarks for PANoptosis. Moreover, ZBP1-mediated PANoptosis occurs in the aortic tissues of TAAD patients. These results highlight the significant role of PANoptosis in TAAD pathogenesis, suggesting ZBP1 and other PANoptosis-related genes as potential therapeutic targets for this condition.
胸主动脉瘤和夹层(TAAD)是一种破坏性的大血管疾病,其发病机制尚未得到充分阐明。本研究旨在探讨新定义的程序性细胞死亡(PCD)——PANoptosis 在 TAAD 发病机制中的作用,其特征为细胞焦亡、细胞凋亡和坏死性凋亡。我们发现,在β-氨基丙腈(BAPN)+血管紧张素 II(Ang II)诱导的 TAAD 小鼠中,起始因子 Z-DNA 结合蛋白 1(ZBP1)和 PANoptosis 相关基因的表达上调。Ang II 刺激增强了 ZBP1 的表达,促进了生物活性 GSDMD(Gasdermin D)片段的产生、Caspase 3 的切割,并增加了人主动脉血管平滑肌细胞(HASMCs)中混合谱系激酶结构域样伪激酶(MLKL)的磷酸化,表明 PANoptosis 的标志性事件发生。此外,ZBP1 介导的 PANoptosis 发生在 TAAD 患者的主动脉组织中。这些结果突出了 PANoptosis 在 TAAD 发病机制中的重要作用,提示 ZBP1 和其他 PANoptosis 相关基因可能是这种疾病的潜在治疗靶点。