Arteriosclerosis, thrombosis, and vascular biology · 2026
Hypertriglyceridemia Does Not Worsen Thoracic Aortic Aneurysm and Dissection in GPIHBP1 Knockout Mice-Brief Report.
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Wang Banglong, Meng Zhe, Li Jiatian, Wu Feng, Song Baoshen, Huang Wei, Liao Jiawei
Аннотация
BACKGROUND: Hypertriglyceridemia is an established risk factor for atherosclerotic cardiovascular disease and has recently been implicated in abdominal aortic aneurysm pathogenesis. However, its role in thoracic aortic aneurysm and dissection (TAAD) remains undefined.
METHODS: We investigated the impact of hypertriglyceridemia on experimental TAAD using GPIHBP1 (glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1) knockout mice as a hypertriglyceridemia model. TAAD was induced in 3- to 4-week-old mice via oral β-aminopropionitrile administration for 28 days.
RESULTS: Despite progressive hypertriglyceridemia in GPIHBP1 knockout mice during β-aminopropionitrile treatment, no significant differences in TAAD incidence, mortality, or the ratio of affected aortic segments to aortic full length were observed between GPIHBP1 knockout mice and their wild-type littermates. Histopathologic and molecular analyses revealed comparable elastin fragmentation, ECM (extracellular matrix) degradation, vascular smooth muscle cell phenotypic transition, and inflammatory cell infiltration in thoracic aortas of both genotypes. These results remained consistent across sexes and different β-aminopropionitrile dosing regimens.
CONCLUSIONS: Our findings demonstrate that hypertriglyceridemia does not significantly exacerbate the development or progression of β-aminopropionitrile-induced TAAD in GPIHBP1-deficient mice.
METHODS: We investigated the impact of hypertriglyceridemia on experimental TAAD using GPIHBP1 (glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1) knockout mice as a hypertriglyceridemia model. TAAD was induced in 3- to 4-week-old mice via oral β-aminopropionitrile administration for 28 days.
RESULTS: Despite progressive hypertriglyceridemia in GPIHBP1 knockout mice during β-aminopropionitrile treatment, no significant differences in TAAD incidence, mortality, or the ratio of affected aortic segments to aortic full length were observed between GPIHBP1 knockout mice and their wild-type littermates. Histopathologic and molecular analyses revealed comparable elastin fragmentation, ECM (extracellular matrix) degradation, vascular smooth muscle cell phenotypic transition, and inflammatory cell infiltration in thoracic aortas of both genotypes. These results remained consistent across sexes and different β-aminopropionitrile dosing regimens.
CONCLUSIONS: Our findings demonstrate that hypertriglyceridemia does not significantly exacerbate the development or progression of β-aminopropionitrile-induced TAAD in GPIHBP1-deficient mice.