目前临床上对小腹主动脉瘤（sAAA）尚无有效干预手段。硫氧还原蛋白相互作用蛋白（TXNIP）与NLRP3结合，激活巨噬细胞炎症小体介导的动脉壁慢性炎症在AAA进展中有重要作用。前期发现，脂肪干细胞外泌体（ADSC-Exo）可显著抑制AAA小鼠瘤壁巨噬细胞炎症小体活化和AAA扩张；ADSC-Exo处理的sAAA患者原代巨噬细胞miR-17-5p水平升高，其靶基因TXNIP水平下降。提出假说：ADSC-Exo可传递miR-17-5p并通过TXNIP-NLRP3途径调控巨噬细胞炎症小体活化、抑制sAAA进展。本项目聚焦ADSC-Exo调控炎症小体活化、抑制sAAA进展的具体机制，拟构建miR-17-5p敲除/过表达的ADSC，在细胞/整体、临床/动物水平阐明ADSC-Exo通过miR-17-5p-TXNIP-NLRP3途径抑制巨噬细胞炎症小体激活、sAAA进展的机制，为干预sAAA提供新思路。

At present, there is no effective intervention for small abdominal aortic aneurysm (sAAA). The binding of thioredoxin interacting protein (TXNIP) to NLRP3, which activates macrophage inflammasome -mediated chronic inflammation of the arterial wall, plays an important role in the progression of AAA. We previously found that adipose-derived stem cell exosomes (ADSC-Exo) significantly inhibited inflammasome activation of macrohages and AAA expansion in AAA mouse; ADSC-Exo-treated macrophages derived from sAAA patients showed increased miR-17-5p levels, companioned with the decreased expression of its target gene TXNIP. We hypothsized that ADSC-Exo can transfer miR-17-5p and regulate macrophage inflammasome activation through TXNIP-NLRP3 pathway to inhibit sAAA progression. This project focuses on the specific mechanism by which ADSC-Exo regulates macrophages inflammasome activation in inhibiting progression of sAAA, we establish miR-17-5p knockout/overexpressing ADSC to elucidate ADSC-Exo inhibits the activation of macrophage inflammasome and thus inhibits the progression of sAAA, via 17-5p-TXNIP-NLRP3 pathway at the cell/overall, clinical/animal level, providing new insights for intervention of sAAA.