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Updated: Jun 7, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
Published on: May 31, 2016
Role of macrophages in vascular calcification: From the perspective of homeostasis
Rong Dong1, Zhenjun Ji2, Mi Wang2
1Department of Cardiology, Zhongda Hospital, School of Medicine, Southeast University, No. 87, Dingjiaqiao, Nanjing 210009, China; Department of Cardiology, Yancheng No. 1 People's Hospital, No. 66 South Renmin Road, Yancheng 224000, China.
Insights
Vascular calcification (VC), a silent condition linked to aging, involves inflammation and macrophages. Targeting these cells offers new therapeutic strategies for cardiovascular and cerebrovascular diseases.
Area of Science:
- Cardiovascular Biology
- Immunology
- Vascular Biology
Background:
- Vascular calcification (VC) is a significant risk factor for cardiovascular and cerebrovascular diseases, with incidence increasing due to global population aging.
- VC often progresses silently, leading to irreversible clinical outcomes.
- Inflammation is central to VC, with macrophages being key inflammatory cells.
Purpose of the Study:
- To review the multifaceted role of macrophages in vascular calcification.
- To explore macrophage heterogeneity and its impact on VC development and regression.
- To discuss therapeutic strategies targeting macrophages for VC prevention and treatment.
Main Methods:
- Literature review summarizing macrophage origins, distribution, classification, and surface markers.
- Exploration of macrophage-mediated mechanisms in VC, including inflammatory factors, osteogenic genes, extracellular vesicles, and efferocytosis.
- Discussion of current research on targeting inflammation and macrophages for VC.
Main Results:
- Macrophages exhibit significant heterogeneity, influencing the occurrence, progression, and regression of VC.
- Macrophage functions in VC involve releasing inflammatory factors, osteogenic genes, and extracellular vesicles, alongside altered efferocytosis.
- Understanding macrophage roles provides insights into VC pathogenesis.
Conclusions:
- Macrophages are critical regulators of vascular calcification through diverse mechanisms.
- Targeting inflammation and specific macrophage functions presents a promising therapeutic avenue for VC.
- Further research into macrophage biology is essential for developing novel treatments for VC.
Abstract:
Vascular calcification (VC) is a crucial risk factor for the high morbidity and mortality associated with cardiovascular and cerebrovascular diseases. With the global population aging, the incidence of VC is escalating annually. However, due to its silent clinical process, VC often results in irreversible clinical outcomes. Inflammation is a core element in the VC process, and macrophages are the major inflammatory cells. Due to their diverse origins, microenvironments, and polarization states, macrophages exhibit significant heterogeneity, exerting strong effects on the occurrence, development, and even the regression of VC. In this review, we summarize the origin, distribution, classification, and surface markers of macrophages. Simultaneously, we explore the mechanisms by which macrophages maintain homeostasis or regulate inflammation, including the macrophage-mediated regulation of VC through the release of inflammatory factors, osteogenic genes, extracellular vesicles, and alterations in efferocytosis. Finally, we discuss research targeting inflammation and macrophages to develop novel therapeutic regimens for preventing and treating VC.
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