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.

PubMed

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.

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