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Updated: Jul 17, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Is inflammation the link between atherosclerosis and vascular calcification in chronic kidney disease?
1Department of Nephrology, General Hospital of Athens, Athens, Greece. tsipg@ath.forthnet.gr
Insights
Vascular calcification in chronic kidney disease (CKD) may be an active inflammatory process, not just a passive consequence. This finding suggests atherosclerosis and vascular calcification are interconnected, potentially sharing common inflammatory pathways.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Inflammation Research
Background:
- Atherosclerosis and vascular calcification frequently coexist in patients with chronic kidney disease (CKD).
- Vascular calcification has traditionally been considered a passive process, unlike the recognized inflammatory nature of atherosclerosis.
- Emerging evidence suggests vascular calcification may also be an active inflammatory process linked to atherosclerosis.
Purpose of the Study:
- To explore the potential role of vascular calcification as an active player in atherosclerosis.
- To investigate the interconnected inflammatory pathways linking vascular calcification and atherosclerosis in CKD.
Main Methods:
- Review of experimental data on vascular calcification and atherosclerosis.
- Analysis of the roles of key molecular factors such as RANKL (receptor activator of nuclear factor kappaB ligand), RANK, and osteoprotegerin.
- Examination of the interaction between basic calcium phosphate crystals, monocytes-macrophages, and inflammatory cytokine production.
Main Results:
- Factors like RANKL, RANK, and osteoprotegerin are implicated in both vascular calcification and atherosclerosis.
- Basic calcium phosphate crystals can activate inflammatory pathways in monocytes-macrophages, potentially initiating atherosclerosis.
- Vascular calcification may actively contribute to the atherosclerotic process rather than being a passive bystander.
Conclusions:
- Vascular calcification might be an active participant in the development of atherosclerosis.
- Inflammation appears to be a common mechanism linking vascular calcification and atherosclerosis in CKD patients.
- Future studies confirming these findings could lead to integrated therapeutic strategies for both conditions in CKD.
Abstract:
Atherosclerosis and vascular calcification often co-exist in chronic kidney disease (CKD) patients. Although the former has been recently recognized as an active inflammatory process, atherosclerosis-related calcification of the intima is still viewed as a passive epiphenomenon. Recent experimental data showed that ossification of the internal vascular wall might also be an active inflammatory process interrelated to atherosclerosis. Factors like RANKL (receptor activator of nuclear factor kappaB ligand), RANK and osteoprotegerin modulate vascular calcification and at the same time are involved in the process of atherosclerosis. Moreover, basic calcium phosphate crystals could interact with and activate monocytes-macrophages that produce proinflammatory cytokines capable of initiating - via endothelial activation and leukocyte adhesion - the atherosclerotic process. Thus, vascular calcification might be an active player and not simply an epiphenomenon in atherosclerosis. Should the above-mentioned data be confirmed in future studies, calcification of the internal vascular wall and atherosclerosis might be viewed and treated as tightly interconnected and linked by inflammation processes in CKD patients.
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Atherosclerosis I: Introduction
Coronary Artery Disease II: Pathophysiology
Chronic Kidney Disease I: Introduction
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Chronic Kidney Disease II: Clinical Manifestations
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