Role of CX3CR1 receptor in monocyte/macrophage driven neovascularization.

It is tempting to speculate whether failure of CX 3 CR1 deficient cells to tubulate, or initiate differentiation into mural smooth muscle-like cells or impairment of extracellular matrix production may be significant contributors to increased microvessel porosity to blood and solutes in vivo thus providing a mechanism underlying the leaky MV phenotype.

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