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Published on: June 2, 2022
[Pathophysiological mechanisms of vascular calcification]
Lucie Hénaut1, Romuald Mentaverri2, Sophie Liabeuf3
1Unité Inserm 1088 : MP3CV « Mécanismes physiopathologiques, causes et conséquences des calcifications vasculaires ». Université de Picardie Jules Verne, France.
Insights
Vascular calcification (VC) is a degenerative vessel wall disease linked to aging and chronic conditions. This review details the active cellular processes and key regulators involved in VC formation.
Area of Science:
- Cardiovascular Biology
- Pathology
- Biomineralization
Context:
- Vascular calcification (VC) is a degenerative arterial disease associated with aging, atherosclerosis, diabetes, and chronic kidney disease.
- VC significantly increases the risk of mortality and cardiovascular disease.
- Previously viewed as passive mineral precipitation, VC is now understood as an active, regulated cellular process.
Purpose:
- To review current knowledge on the mechanisms of vascular calcification.
- To detail the roles of key cellular actors modulating VC formation.
Summary:
- Vascular calcification involves active, regulated cellular processes similar to bone formation.
- Key cellular and molecular pathways drive the development of VC.
- Understanding these mechanisms is crucial for therapeutic development.
Impact:
- Provides a comprehensive overview of VC pathogenesis.
- Highlights the cellular basis of vascular calcification.
- Informs future research into preventing and treating VC and its cardiovascular consequences.
Abstract:
Vascular calcification (VC) is a degenerative pathology of the vessel wall. In the general population, VC appearance is associated with aging, but this pathology can also develop as a consequence of atherosclerosis, diabetes, inflammatory and chronic kidney disease. VC is strongly associated with increased risk of mortality and cardiovascular disease. Although VC has long been considered as the result of a passive precipitation of mineral, it is now well established that this pathology results from an active and highly regulated cellular process, which shares similarities with bone formation. This review summarizes our current knowledge on VC formation, and details the modalities of action of the main actors known to modulate this process.
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