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Updated: Jan 13, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Iron in Vascular Calcification: Pro-Calcific Agent or Protective Modulator?
Enikő Balogh1, Andrea Tóth1, Viktória Jeney1
1Vascular Pathophysiology Research Group, Research Centre for Molecular Medicine, Faculty of Medicine, University of Debrecen, 4032 Debrecen, Hungary.
Insights
Iron metabolism disturbances impact vascular calcification, a key factor in cardiovascular disease. This review explores iron
Area of Science:
- Cardiovascular Biology
- Mineral Metabolism
- Vascular Biology
Background:
- Vascular calcification contributes to cardiovascular disease, especially in chronic kidney disease (CKD) and diabetes.
- It's an active, cell-mediated process resembling bone formation.
- Iron metabolism is a newly identified modulator of vascular calcification.
Purpose of the Study:
- To review the dual role of iron in vascular calcification.
- To summarize in vitro and in vivo studies on iron's impact on vascular cell calcification.
- To explore clinical evidence linking iron metabolism to coronary artery calcification in CKD.
Main Methods:
- Literature review of in vitro and in vivo studies.
- Analysis of mechanistic insights into iron's role.
- Compilation of clinical data on iron metabolism and vascular calcification in CKD.
Main Results:
- Iron has a complex, dose-dependent role in vascular calcification.
- Studies show iron can both promote and inhibit vascular cell calcification.
- Clinical data links altered iron metabolism to increased coronary artery calcification and mortality in CKD.
Conclusions:
- Iron metabolism is a critical factor in vascular calcification.
- Understanding iron's dual role is essential for managing cardiovascular risk in CKD patients.
- Further research is needed to elucidate iron's precise mechanisms in vascular calcification.
Abstract:
Vascular calcification is a complex, regulated process characterized by the pathological deposition of calcium phosphate minerals in the vascular wall, contributing to cardiovascular morbidity and mortality, particularly in patients with chronic kidney disease (CKD), diabetes, and aging. Once thought to be a passive degenerative process, it is now recognized as an active, cell-mediated phenomenon that shares molecular features with bone formation. Beyond traditional risk factors such as hyperphosphatemia and inflammation, disturbances in iron metabolism have recently emerged as modulators of vascular calcification. Iron, a vital trace element involved in numerous cellular functions, exhibits a dual role as both a potential driver and inhibitor of calcification, depending on its dose, distribution, and cellular context. In this review, we summarize in vitro and in vivo studies investigating the impact of iron on the osteochondrogenic differentiation and calcification of vascular smooth muscle cells and valve interstitial cells. We further highlight mechanistic insights that may explain the divergent findings reported in the literature. Finally, we compile clinical evidence linking disturbances in iron metabolism with coronary artery calcification and cardiovascular mortality in CKD patients.
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