Key result
PDE1C promotes vascular smooth muscle cell proliferation by inhibiting growth factor receptor degradation.
May suggest PDE1C inhibition to limit vascular remodeling; leaves open clinical translation in atherosclerosis or restenosis.
T he endothelium regulates the contractile status of vascular smooth muscle cells (VSMCs). 1 The interaction between endothelial cells (ECs) and VSMCs plays an important role in regulating vascular homeostasis.ECs release vasoactive factors, such as prostacyclin, (nitric oxide [NO]), and endothelium-derived hyperpolarizing factor, which participate in the regulation of vascular tone. 1 Endothelial dysfunction induces the increased expression of adhesion molecules for inflammatory cells.Accumulated inflammatory cells generate an oxidizing environment, which involves abundant reactive oxygen species, inflammatory cytokines/chemokines, and growth factors that contribute to VSMC phenotypic modulation. 2 Thus, EC damage is a trigger underlying VSMC phenotypic change and pathological vascular remodeling.
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Satoh et al. (2015) studied Vascular remodeling. PDE1C was evaluated. PDE1C negatively regulates growth factor receptor degradation and promotes vascular smooth muscle cell proliferation.
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