Wang Zhaomeng, Zhang Haoran, Xie Zhanxiong, Xiang Yukun, Fu Yiwen, Wang Zixun, Jiao Haiqing, Lin Nan, Niu Chenguang, Jiang Chao, Zheng Lemin
Beijing Tiantan Hospital, China National Clinical Research Center for Neurological Diseases, Advanced Innovation Center for Human Brain Protection, Beijing Institute of Brain Disorders, the Capital Medical University, Beijing, China.
The Second School of Clinical Medicine, Southern Medical University, Guangzhou, Guangdong, China.
J Cell Mol Med. 2026 Jan;30(1):e70971. doi: 10.1111/jcmm.70971.
Aortic dissection is a life-threatening cardiovascular emergency with limited pharmacological options. This study focuses on elucidating the multi-target and multi-pathway mechanisms through which morusin mitigates aortic dissection progression, integrating network pharmacology, single-cell transcriptomics and experimental validation. Multi-database analysis identified 281 morusin targets and 1741 ad-related genes, with 84 overlaps. Enrichment analyses highlighted IL-17, HIF-1 and MAPK signalling pathways as potential regulatory hubs. Protein-protein interaction network analysis identified seven key targets, all showing high binding affinity to morusin in molecular docking. Single-cell transcriptomics revealed cell-type-specific dysregulation, notably MAPK8 upregulation in fibroblasts and immune cells. In vitro, morusin dose-dependently inhibited AngII-induced vascular smooth muscle cell proliferation and modulated IL-17 pathway gene expression. In vivo, morusin attenuated aortic dilation and reduced morbidity and mortality in a BAPN-induced AD mouse model. These findings suggest that morusin mitigates AD progression by targeting key inflammatory and apoptotic pathways, supporting its potential as a multi-target therapeutic candidate.
主动脉夹层是一种危及生命的心血管急症,药物治疗选择有限。本研究聚焦于阐明桑色素减轻主动脉夹层进展的多靶点和多途径机制,整合了网络药理学、单细胞转录组学和实验验证。多数据库分析确定了281个桑色素靶点和1741个与主动脉夹层相关的基因,其中有84个重叠。富集分析突出了IL-17、HIF-1和MAPK信号通路作为潜在的调控枢纽。蛋白质-蛋白质相互作用网络分析确定了七个关键靶点,在分子对接中均显示出与桑色素的高结合亲和力。单细胞转录组学揭示了细胞类型特异性失调,尤其是成纤维细胞和免疫细胞中MAPK8的上调。在体外,桑色素剂量依赖性地抑制血管紧张素II诱导的血管平滑肌细胞增殖,并调节IL-17途径基因表达。在体内,桑色素减轻了主动脉扩张,并降低了苯肾上腺素诱导的主动脉夹层小鼠模型的发病率和死亡率。这些发现表明,桑色素通过靶向关键的炎症和凋亡途径减轻主动脉夹层进展,支持其作为多靶点治疗候选药物的潜力。