Vascular remodeling

Vascular remodeling encompasses dynamic structural adaptations in blood vessels, driven by endothelial sensing of fluid shear stress, biomechanical cues, and inflammatory signals, leading to changes in lumen diameter, wall composition, and cellular phenotypes involving endothelial cells, vascular smooth muscle cells, pericytes, fibroblasts, and infiltrating immune cells. In physiology, it ensures network stability during embryogenesis, growth, and exercise by restoring shear stress set points via pathways like VEGFR3 mechanotransduction, which differentiates arterial-venous identities and regulates angiogenesis. Pathologically, dysregulated remodeling contributes to hypertension through resistance vessel narrowing, atherosclerosis via plaque growth and instability from chemokine-driven monocyte infiltration (e.g., CCL2, CCL5), and pulmonary hypertension via hypoxic signaling like HIF-2α. It also underlies post-injury responses such as in-stent restenosis or graft failure, where VSMC proliferation and matrix metalloproteinases degrade stability. While not druggable as a single entity, therapeutic strategies target upstream regulators—such as chemokine blockers (CCL19/CCL21) to reduce foam cell formation or VEGF modulators for angiogenesis control—offering potential to stabilize plaques or enhance regeneration, though challenges include balancing adaptive versus maladaptive responses to avoid ischemia or excessive fibrosis

Other names

Vascular remodelling (British spelling)vessel remodeling

Process modulated indirectly; e.g., VEGFR3 signaling adjusts shear stress set point to trigger outward/inward remodeling; inflammatory chemokines like CCL19/CCL21 promote VSMC proliferation and plaque instability