The Role of Immune Cells and Inflammatory Proteins in Aortic Dissection

Announcing a new article publication for Cardiovascular Innovations and Applications journal. Aortic dissection (AD) is one of the most life-threatening emergencies in cardiovascular diseases, with mortality rates increasing by 1%-2% per hour in untreated Stanford type A AD patients, exceeding 55% within 48 hours. Therefore, investigating the mechanisms underlying AD pathogenesis and developing effective interventions are critically important. The pathological changes in AD primarily result from degeneration of the aortic media, leading to loss of elasticity and reduced resistance to mechanical stress, ultimately causing rupture of the medial layer and formation of a false lumen.

Historically, research on AD pathogenesis has focused on both genetic and non-genetic factors in humans and mice: genetic factors such as Marfan syndrome and Loeys-Dietz syndrome that induce structural abnormalities in the aortic wall, and non-genetic factors including abnormal wall shear stress and hemodynamic disturbances caused by hypertension.

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Songhao Jia, Yang Zhang and Houzao Chen. The Role of Immune Cells and Inflammatory Proteins in Aortic Dissection. CVIA. 2025. Vol. 10(1). DOI: 10.15212/CVIA.2025.0027

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