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Iron deficiency promotes intra-leaflet hemorrhage-induced aortic valve calcification: an experimental study

Huiruo Liu1,2,3,4,5, Zeyu Yang1,2,3,4,5, Hourong Sun6

  • 1Department of Emergency Medicine, Qilu Hospital of Shandong University, Jinan, China.

International Journal of Surgery (London, England)
|December 27, 2024
PubMed

Insights

Iron deficiency (ID) exacerbates calcified aortic valve disease (CAVD) by increasing iron overload in valve cells, promoting fibrosis and calcification. Monitoring and correcting ID may help slow CAVD progression.

Area of Science:

  • Cardiovascular Research
  • Iron Metabolism
  • Valvular Heart Disease

Background:

  • Intra-leaflet hemorrhage (IH) is detrimental in calcified aortic valve disease (CAVD).
  • Iron deficiency (ID) is a common comorbidity in CAVD and may influence IH-induced responses.
  • The role of ID in IH-mediated fibro-osteogenic differentiation of valvular interstitial cells (VICs) was investigated.

Purpose of the Study:

  • To investigate the relationship between ID and pathological changes in CAVD.
  • To determine the effects of ID on IH-mediated fibro-osteogenic differentiation of VICs.

Main Methods:

  • Analysis of 2495 patients in a discovery study and 34 in a validation study.
  • Immunofluorescence and Western blot analyses to assess TFR1 expression.
  • Perl's staining for iron accumulation.
  • In vitro studies using VICs cultured with serum from ID patients.

Main Results:

  • ID was associated with CAVD severity and progression, particularly in an age-dependent manner.
  • TFR1 was significantly upregulated in human calcified aortic valves.
  • Iron accumulation and fibro-calcific differentiation were observed in VICs exposed to ID patient serum.

Conclusions:

  • ID triggers TFR1-mediated iron overload in human VICs, leading to fibrosis and calcification.
  • This process contributes to IH-mediated valve remodeling and calcification in CAVD.
  • Monitoring and correcting ID may be a potential strategy to slow or prevent valvular calcification progression.
Abstract

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