Central to this pathological process is the phenotypic switching of vascular smooth muscle cells (VSMCs) from a quiescent contractile state to a proliferative, migratory, and synthetic phenotype.
First-pass extracted concept
vascular smooth muscle cell phenotypic switching
Aliases
phenotypic switching of vascular smooth muscle cells, VSMCs phenotypic switching
Evidence Snippets
Supporting Sources
Linked Claims
The complexity of vascular smooth muscle cell regulatory networks and the limitations of current interventions support a need for integrative approaches combining molecular targeting with innovative delivery systems.
Vascular smooth muscle cell phenotypic switching is a central mechanism in vein graft intimal hyperplasia.
PDGF-BB, TGF-β, MAPK, mTOR, NF-κB, and non-coding RNAs are described as key regulators of vascular smooth muscle cell phenotypic switching in vein graft intimal hyperplasia.
In vein graft pathology, vascular smooth muscle cells switch from a quiescent contractile state to a proliferative, migratory, and synthetic phenotype.