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Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

Cell-matrix mechanics and pattern formation in inflammatory cardiovascular calcification

Jeffrey J Hsu¹, Jina Lim², Yin Tintut³

¹Department of Medicine, Division of Cardiology, University of California, Los Angeles (UCLA), Los Angeles, California, USA.

Heart (British Cardiac Society)

|July 14, 2016

Insights

Cardiovascular calcific diseases involve vascular cells interacting with their matrix. This interaction, influenced by biomechanics and inflammation, mirrors bone development, driving pathological mineralization.

Area of Science:

Cardiovascular Biology
Biomaterials Science
Cellular Mechanobiology

Background:

Calcific diseases like atherosclerosis and aortic valve disease are major causes of morbidity and mortality.
Vascular cells interact with the extracellular matrix (ECM) via molecular and biomechanical signals, similar to bone cells.
Pathological mineralization in arteries and valves is strongly influenced by contractile vascular cells and their matrix interactions.

Purpose of the Study:

To review the roles of ECM proteins and biomechanics in inflammatory cardiovascular calcification.
To highlight the parallels between cardiovascular calcification and embryonic bone development.
To explore how matrix characteristics and inflammation influence vascular cell behavior and differentiation.

Main Methods:

Literature review synthesizing findings on ECM proteins, biomechanics, and cellular signaling in cardiovascular calcification.
Analysis of mechanisms linking cellular biomechanics (e.g., cytoskeletal forces) to matrix-mediated cell differentiation.
Examination of the interplay between inflammation, ECM properties, and cellular responses.

Main Results:

ECM proteins create microenvironments that support crystal growth and provide mechanical cues for cell differentiation.
Cellular sensing of matrix stiffness via integrin-mediated signaling can trigger differentiation, involving factors like TGF-β superfamily members.
Inflammation and ECM characteristics are interconnected, with inflammation altering the ECM and matrix properties modulating cellular sensitivity to cytokines.

Conclusions:

The interaction between contractile vascular cells and their matrix is a key driver of pathological cardiovascular mineralization.
Understanding the biomechanical and molecular signaling within the ECM is crucial for developing therapeutic strategies against cardiovascular calcification.
The review underscores the complex interplay of matrix composition, mechanical properties, and inflammatory processes in the pathogenesis of vascular and valvular calcification.

Read full analysis

Abstract:

Calcific diseases of the cardiovascular system, such as atherosclerotic calcification and calcific aortic valve disease, are widespread and clinically significant, causing substantial morbidity and mortality. Vascular cells, like bone cells, interact with their matrix substrate through molecular signals, and through biomechanical signals, such as traction forces transmitted from cytoskeleton to matrix. The interaction of contractile vascular cells with their matrix may be one of the most important factors controlling pathological mineralisation of the artery wall and cardiac valves. In many respects, the matricrine and matrix mechanical changes in calcific vasculopathy and valvulopathy resemble those occurring in embryonic bone development and normal bone mineralisation. The matrix proteins provide a microenvironment for propagation of crystal growth and provide mechanical cues to the cells that direct differentiation. Small contractions of the cytoskeleton may tug on integrin links to sites on matrix proteins, and thereby sense the stiffness, possibly through deformation of binding proteins causing release of differentiation factors such as products of the members of the transforming growth factor-β superfamily. Inflammation and matrix characteristics are intertwined: inflammation alters the matrix such as through matrix metalloproteinases, while matrix mechanical properties affect cellular sensitivity to inflammatory cytokines. The adhesive properties of the matrix also regulate self-organisation of vascular cells into patterns through reaction-diffusion phenomena and left-right chirality. In this review, we summarise the roles of extracellular matrix proteins and biomechanics in the development of inflammatory cardiovascular calcification.

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