Journal
NUTRIENTS
Volume 15, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/nu15071640
Keywords
thoracic aortic dissection; low zinc; inflammation; vascular smooth muscle cells; phenotypic transition
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Low zinc can reduce the development of thoracic aortic dissection triggered by vascular inflammation. It achieves this by reducing the infiltration of macrophages, inhibiting the expression of inflammatory cytokines, suppressing the phenotype switch of vascular smooth muscle cells, and ultimately improving the progression of thoracic aortic dissection.
Vascular inflammation triggers the development of thoracic aortic dissection (TAD). Zinc deficiency could dampen tissue inflammation. However, the role of zinc as a nutritional intervention in the progression of TAD remains elusive. In this study, we employed a classical b-aminopropionitrile monofumarate (BAPN)-induced TAD model in mice treated with low zinc and observed that the TAD progression was greatly ameliorated under low zinc conditions. Our results showed that low zinc could significantly improve aortic dissection and rupture (BAPN + low zinc vs. BAPN, 36% vs. 100%) and reduce mortality (BAPN + low zinc vs. BAPN, 22% vs. 57%). Mechanically, low zinc attenuated the infiltration of macrophages and inhibited the expression of inflammatory cytokines, suppressed the phenotype switch of vascular smooth muscle cells from contractile to synthetic types, and eventually alleviated the development of TAD. In conclusion, this study suggested that low zinc may serve as a potential nutritional intervention approach for TAD prevention.
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