ObjectiveTo investigate the pivotal role and key molecular mechanisms of aortic dissection (AD) pathogenesis, providing novel perspectives for early diagnosis and treatment. Methods The relevant literature on domestic and foreign research in recent years was summarized. ResultsVascular aging constitutes a fundamental pathological basis for AD, genic abnormalities (e.g., Gene 33, CEBPB, IGFBP-3) and signal pathway dysregulation(e.g., Notch, ferroptosis) are important to genesis of AD. ConclusionAD pathogenesis is intimately linked to vascular aging. Targeting aging-associated genes or pathways may emerge as innovative strategies for AD prevention and management. Further clinical translational research is warranted to establish the safety and therapeutic efficacy.
