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Abdominal aortic aneurysm (AAA) is a pathological condition characterized by a localized dilation of the abdominal aorta exceeding 3 cm in diameter or 50% larger than normal, resulting from weakening of the aortic wall due to factors like aging, tobacco use, inflammation, and proteolytic degradation of extracellular matrix components. It typically remains asymptomatic until rupture, which presents with severe abdominal or back pain, shock, and high mortality rates. Pathogenesis involves chronic inflammation with infiltration of immune cells such as macrophages, mast cells, and lymphocytes, producing cytokines (e.g., IL-6, IFN-γ, MCP-1) and proteases (e.g., MMPs, chymase, tryptase) that degrade elastin and collagen, leading to vessel wall thinning and expansion. Molecular factors like reactive oxygen species (ROS), TGF-β, and lysyl oxidase (LOX) dysregulation further contribute to smooth muscle cell apoptosis and impaired matrix stability. No specific pharmacological drugs target AAA directly; management focuses on surveillance for small aneurysms and surgical repair (open or endovascular) for larger ones at high rupture risk. Biomarkers such as NGAL and certain HLA genes aid in diagnosis and rupture prediction, but challenges include identifying high-risk subtypes and preventing progression.
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