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Iron deficiency exacerbates aortic medial degeneration by inducing excessive mitochondrial fission

Xiaohan Zhong1,2,3, Qi Wu1,2,3, Zhiwei Wang1,3

  • 1Department of Cardiothoracic Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, People's Republic of China. wangzhiwei@whu.edu.cn.

Food & Function
|June 23, 2022
PubMed

Insights

Iron deficiency accelerates aortic medial degeneration by promoting mitochondrial fission and vascular smooth muscle cell transformation. Maintaining iron balance may prevent aortic aneurysm and dissection.

Area of Science:

  • Cardiovascular Biology
  • Nutritional Science
  • Mitochondrial Biology

Background:

  • Iron deficiency (ID) is linked to aortic aneurysm and dissection (AAD) pathogenesis.
  • Mitochondrial dynamics influence vascular smooth muscle cell (VSMC) apoptosis and transformation.
  • The role of mitochondrial dynamics in ID-induced aortic medial degeneration (AMD) remains unclear.

Purpose of the Study:

  • To investigate the impact of ID on VSMC phenotypic transformation and AMD progression.
  • To elucidate the underlying mechanisms, focusing on mitochondrial dynamics.

Main Methods:

  • Analysis of p-Drp1 and Fis1 expression in AAD patients and AngII-infused ApoE-/- mice.
  • Assessment of mitochondria-associated endoplasmic reticulum membranes (MAMs) formation.
  • Evaluation of Drp1 inhibitor effects on AMD progression.

Main Results:

  • p-Drp1 (Ser616) and Fis1 were upregulated in AAD.
  • ID promoted MAMs formation and excessive mitochondrial fission.
  • This process induced VSMC transformation and accelerated AMD.
  • A Drp1 inhibitor partially reversed these effects.

Conclusions:

  • ID promotes AMD by enhancing mitochondrial fission and VSMC transformation.
  • Targeting Drp1 may offer a therapeutic strategy for AAD.
  • Maintaining iron homeostasis is crucial for preventing AAD development.

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