文章标题：Fosb promotes ferroptosis in vascular smooth muscle cells via the NF-κB pathway to exacerbate abdominal aortic aneurysm progression

作者列表：Xiang Li, Qing Wang, Jiecheng Zhang, Wenjun Zhao, Xinting Zheng

影响因子：3.7

期刊：CELLULAR SIGNALLING

发表时间：2026-4-19

DOI:10.1016/j.cellsig.2026.112544

文献主题：Abstract

Background

Abdominal aortic aneurysm (AAA) is a fatal disease characterized by vascular wall inflammation and matrix remodeling. The inflammatory phenotypic transｆormation of smooth muscle cells (SMCs) holds a pivotal role in AAA pathogenesis. As an inflammatory regulator, whether FBJ osteosarcoma oncogene B (Fosb) participates in AAA progression by driving SMC phenotypic switching remains unclear.

Methods

Using the scRNA-seq data from AAA patients, we identified Fosb as a key driver of SMC phenotypic switching through cell clustering annotation, differential gene screening, functional enrichment, and pseudo-time trajectory analysis. An in vitro AAA cell model was established using Ang-II-stimulated T/G HA-VSMC cells. Fosb expression was assessed by qRT-PCR and western blot (WB). AAA cell models with Fosb knockdown or overexpression were constructed to investigate the effects of Fosb on T/G HA-VSMC cell proliferation, apoptosis, migration, invasion, contractile marker protein expression, and inflammatory cytokine secretion via WB, CCK8, Transwell, flow cytometry, and ELISA. Furthermore, WB was applied in detecting ferroptosis and NF-κB signaling pathway protein expression. Kits were employed for the determination of MDA, GSH, and Fe2+ levels, and flow cytometry was for ROS levels. Finally, an Ang-II-induced ApoE−/− mouse AAA model was constructed, and histological staining, WB, IHC, and ELISA were carried out to validate that Fosb boosted AAA ferroptosis and inflammation via the NF-κB pathway in vivo.