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.