ALDH(2) knockout protects against aortic dissection

BACKGROUND: The incidence and mortality of aortic dissection (AD) are increasing. In pathological studies, macrophages, T lymphocytes and dendritic cells were found in the tunica media of the aorta. Acetaldehyde dehydrogenase 2 (ALDH(2)) gene polymorphisms are associated with a high incidence of hypertension in Asian populations. However, there is no clear evidence of the relationship between ALDH(2) and aortic dissection in Asians. The aim of this study was to investigate the incidence of aortic dissection in different ALDH(2) genotypes and explore changes in the vasculature. MATERIALS AND METHODS: Three-week-old male mice were administered freshly prepared β-aminopropionitrile solution dissolved in drinking water (1 g/kg/d) for 28 days to induce TAD. An animal ultrasound imaging system was used to observe the formation of arterial dissection and changes in cardiac function. Subsequently, mice were euthanized by cervical dislocation. The aortas were fixed for HE staining and EVG staining to observe aortic elastic fiber tears and pseudoluma formation under a microscope. RESULTS: Knockout of ALDH(2) mitigated β-aminopropionitrile-induced TAD formation in animal studies. Ultrasound results showed that ALDH(2) knockout reduced the degree of ascending aortic widening and the incidence of aortic dissection rupture. Pathological sections of multiple aortic segments showed that the protective effect of ALDH(2) knockout was observed in not only the ascending aorta but also the aortic arch and descending aorta. The expression levels of genes related to NK CD56bright cells, Th17 cells, T cells and T helper cells were decreased in ALDH(2) knockout mice treated with β-aminopropionitrile for 28 days. CONCLUSION: ALDH(2) knockout protects against aortic dissection by altering the inflammatory response and immune response and protecting elastic fibers.