中性粒细胞炎性反应在腹主动脉瘤发病机制中的研究进展

腹主动脉瘤（AAA）是成年人主动脉破裂导致死亡的重要原因，其发病机制尚未完全阐明，且缺乏切实有效的药物治疗手段。作为先天免疫系统的首要防线，中性粒细胞在循环系统白细胞中占据70%的比例。中性粒细胞可通过吞噬、脱颗粒、产生活性氧以及形成中性粒细胞胞外诱捕网（NETs）等机制，参与炎症反应。多项研究表明，中性粒细胞参与无菌性炎症和血栓形成，且过度活化的中性粒细胞也可杀伤正常组织和细胞，造成疾病发生，与AAA的发生发展密切相关。本文结合AAA细胞外基质降解、炎性浸润和血管平滑肌细胞功能丧失三大病理特征，深入探讨了中性粒细胞在AAA病程中的多重角色。中性粒细胞通过炎症因子等机制被募集至病变部位，造成炎性浸润，活化后释放杀伤酶类、基质金属蛋白酶等分子，促进AAA的发展；中性粒细胞通过细胞沉积及相关炎性分子的累积，参与AAA腔内血栓形成，加重疾病进展；中性粒细胞形成NETs为近年来新发现的中性粒细胞杀伤形式，已有文献报道NETs从多角度协同加重炎症，且可能通过激活凝血级联、促进血小板聚集等方式形成腔内血栓，导致AAA的病变加剧，对该疾病进展有重要作用。由于相关研究尚处起步，且多数研究结论尚处表层，...

Inflammatory response of neutrophils in the pathogenesis of abdominal aortic aneurysm

Abdominal aortic aneurysm (AAA) is a significant cause of death in adults due to aortic rupture. The pathogenesis of AAA is not fully understood, and there is a lack of reliable and effective pharmacological treatment options. Neutrophils, constituting 70% of circulating white blood cells, serve as the primary defense line of the innate immune system. Neutrophils can participate in the inflammatory response through mechanisms such as phagocytosis, degranulation, the generation of reactive oxygen species, and the formation of neutrophil extracellular traps (NETs). Multiple studies indicate that neutrophils are involved in sterile inflammation and thrombosis, and over-activated neutrophils can also inflict damage on normal tissues and cells, leading to the occurrence of diseases, and this is closely associated with the onset and progression of AAA. This article, integrating the three major pathological features of AAA: extracellular matrix degradation, inflammatory infiltration, and loss of vascular smooth muscle cell function, delves into the multiple roles of neutrophils in the course of AAA. Neutrophils are recruited to the lesion site through mechanisms such as inflammatory factors, causing inflammatory infiltration. Once activated, they release proteolytic enzymes, matrix metalloproteinases, and other molecules, promoting the development of AAA. Neutrophils participate in intraluminal thrombus formation within the AAA by cellular deposition and accumulation of related inflammatory molecules, exacerbating disease progression. The formation of NETs, a recently discovered neutrophil killing mechanism, has been reported to synergistically intensify inflammation from multiple aspects. They may also contribute to intraluminal thrombus formation by activating the coagulation cascade and promoting platelet aggregation, leading to the worsening of AAA lesions. This process plays a crucial role in the progression of this disease. Due to the early stage of related research and the superficial nature of most research conclusions, this article emphasizes the need for a more in-depth understanding within the academic community regarding the complex interactions of neutrophils in the mechanism of AAA, and highlights the significance of elucidating the role of neutrophils in the inflammatory microenvironment of this disease. By providing a comprehensive overview and analysis at the organ, tissue, and cellular levels, this article provides an in-depth reference for experimental research related to AAA. Additionally, it summarizes and discusses potential future research directions, offering insights into the discovery of effective diagnostic and therapeutic targets for AAA.