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Updated: Feb 14, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Vascular Calcification: Is it rather a Stem/Progenitor Cells Driven Phenomenon?
Aleksandra Leszczynska1, J Mary Murphy2
1Regenerative Medicine Institute, Cedars-Sinai Medical Center, Los Angeles, CA, United States.
Insights
Vascular calcification (VC) involves ectopic bone and cartilage formation in atherosclerosis. This review explores the role of progenitor cells in VC pathogenesis, challenging existing theories.
Area of Science:
- Cardiovascular Biology
- Cell Biology
- Vascular Biology
Background:
- Vascular calcification (VC) is a significant factor in atherosclerosis, a leading cause of morbidity and mortality.
- Current theories on VC pathogenesis, including response-to-injury and smooth muscle transdifferentiation, are incomplete.
- The vasculature possesses a remarkable capacity for repair throughout life.
Purpose of the Study:
- To review the role of circulating and resident progenitor cells in vascular calcification.
- To discuss intrinsic cellular mechanisms driving ectopic cartilage and bone formation in atherosclerosis.
Main Methods:
- Literature review focusing on recent advancements in vascular calcification research.
- Analysis of studies investigating progenitor cell involvement in atherogenesis and VC.
Main Results:
- Emerging evidence highlights progenitor cells as key players in VC.
- Intrinsic cellular mechanisms are crucial for determining cell fate in ectopic ossification.
Conclusions:
- Progenitor cell involvement offers a new perspective on VC pathogenesis.
- Further research into cellular mechanisms is needed to fully understand and treat VC in atherosclerosis.
Abstract:
Vascular calcification (VC) has witnessed a surge of interest. Vasculature is virtually an omnipresent organ and has a notably high capacity for repair throughout embryonic and adult life. Of the vascular diseases, atherosclerosis is a leading cause of morbidity and mortality on account of ectopic cartilage and bone formation. Despite the identification of a number of risk factors, all the current theories explaining pathogenesis of VC in atherosclerosis are far from complete. The most widely accepted response to injury theory and smooth muscle transdifferentiation to explain the VC observed in atherosclerosis is being challenged. Recent focus on circulating and resident progenitor cells in the vasculature and their role in atherogenesis and VC has been the driving force behind this review. This review discusses intrinsic cellular players contributing to fate determination of cells and tissues to form ectopic cartilage and bone formation.
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