Cell-Matrix Interactions and Matricrine Signaling in the Pathogenesis of Vascular Calcification

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Vascular calcification is a complex pathological process occurring in patients with atherosclerosis, type 2 diabetes, and chronic kidney disease. The extracellular matrix, via matricrine-receptor signaling plays important roles in the pathogenesis of calcification. Calcification is mediated by osteochondrocytic-like cells that arise from transdifferentiating vascular smooth muscle cells. Recent advances in our understanding of the plasticity of vascular smooth muscle cell and other cells of mesenchymal origin have furthered our understanding of how these cells transdifferentiate into osteochondrocytic-like cells in response to environmental cues. In the present review, we examine the role of the extracellular matrix in the regulation of cell behavior and differentiation in the context of vascular calcification. In pathological calcification, the extracellular matrix not only provides a scaffold for mineral deposition, but also acts as an active signaling entity. In recent years, extracellular matrix components have been shown to influence cellular signaling through matrix receptors such as the discoidin domain receptor family, integrins, and elastin receptors, all of which can modulate osteochondrocytic differentiation and calcification. Changes in extracellular matrix stiffness and composition are detected by these receptors which in turn modulate downstream signaling pathways

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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