Low Zinc Alleviates the Progression of Thoracic Aortic Dissection by Inhibiting Inflammation

Nutrients. 2023 Mar 28;15(7):1640. doi: 10.3390/nu15071640.

Abstract

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 β-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.

Keywords: inflammation; low zinc; phenotypic transition; thoracic aortic dissection; vascular smooth muscle cells.

MeSH terms

  • Aminopropionitrile / adverse effects
  • Animals
  • Aorta, Thoracic
  • Aortic Aneurysm, Thoracic* / chemically induced
  • Aortic Aneurysm, Thoracic* / metabolism
  • Aortic Dissection*
  • Disease Models, Animal
  • Dissection, Thoracic Aorta*
  • Inflammation
  • Mice
  • Zinc / adverse effects

Substances

  • Aminopropionitrile
  • Zinc

Grants and funding

This work was supported by the National Natural Science Foundation of China (31970717, 82170429), the Chinese Universities Scientific Fund (2020TC015), and the Beijing Municipal Natural Science Foundation (7222111).