Thoracic aortic dissection (TAD) is a highly lethal cardiovascular emergency in clinical practice. Its annual incidence stands at approximately 3-4 per 100 000 individuals and is on the rise. This condition confers an extremely poor prognosis. In patients who fail to receive timely treatment, the mortality rate reaches 1%-2% per hour on the first day, rising to 50% within one week, with a recurrence rate of approximately 8.0%, significantly increasing the burden on clinical diagnosis and treatment. In-depth exploration of the pathological mechanisms underlying TAD holds significant research value for elucidating the disease's essence and optimising diagnostic and therapeutic strategies. The pathogenesis and progression of TAD involve multidimensional aetiological factors. This review focuses on the core pathological mechanisms underpinning TAD development, summarising current research advances from multiple perspectives: the biomechanical properties of the aortic wall, smooth muscle cell phenotypic switching and imbalanced extracellular matrix degradation, endothelial dysfunction, inflammatory and immune responses, and genetic susceptibility. It aims to provide a reference framework for both fundamental research and clinical management of TAD.
