The Vicious Cycle of Arterial Stiffness and Arterial Media Calcification

Geoffrey Van den Bergh1, Britt Opdebeeck1, Patrick C D'Haese1

  • 1Laboratory of Pathophysiology, Department of Biomedical Sciences, University of Antwerp, B-2610 Wilrijk, Belgium.

Trends in Molecular Medicine
|September 17, 2019
PubMed

Insights

Arterial media calcification and stiffness predict cardiovascular death. Targeting intimal cells, not just vascular smooth muscle cells, may break the cycle driving these conditions.

Area of Science:

  • Cardiovascular biology
  • Vascular cell biology
  • Pathophysiology of atherosclerosis

Background:

  • Arterial media calcification and arterial stiffness are independent predictors of cardiovascular mortality.
  • These conditions form a vicious cycle involving endothelial and vascular smooth muscle cell transdifferentiation.
  • Endothelial cells initiate this cycle by sensing pathological triggers like aging and inflammation.

Purpose of the Study:

  • To highlight the central role of endothelial and vascular smooth muscle cells in arterial calcification and stiffness.
  • To propose expanding therapeutic targets beyond vascular smooth muscle cells to include intimal layer cells.

Main Methods:

  • Review of existing literature on arterial calcification and stiffness.
  • Analysis of the roles of endothelial and vascular smooth muscle cells in the pathological cycle.
  • Comparative analysis of current therapeutic strategies versus potential new targets.

Main Results:

  • Endothelial cell behavior is crucial for vascular smooth muscle cell function in the arterial media.
  • Endothelial/intimal cells act as primary sensors and initiators of the calcification and stiffness cycle.
  • Current treatments primarily focus on vascular smooth muscle cells, potentially overlooking key initiators.

Conclusions:

  • The vicious cycle of arterial calcification and stiffness is initiated by intimal layer cells.
  • Therapeutic strategies should consider targeting intimal layer cells in addition to vascular smooth muscle cells.
  • A shift in focus to intimal targets may offer novel treatments for cardiovascular mortality reduction.

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