Vascular smooth muscle cell proliferation pathways (VSMC proliferation pathways)

Vascular smooth muscle cell (VSMC) proliferation pathways encompass the integrated network of signaling cascades, such as the MAPK/ERK and PI3K/Akt/mTOR pathways, that regulate the growth and division of smooth muscle cells within the arterial wall [1][5]. In a healthy physiological state, VSMCs exhibit a contractile phenotype to maintain vascular tone, but they can undergo a phenotypic switch to a synthetic, proliferative state in response to vascular injury or inflammatory cytokines like Platelet-Derived Growth Factor (PDGF) [3]. This pathological proliferation is a central mechanism in the development of atherosclerosis, hypertension, and neointimal hyperplasia following clinical procedures like angioplasty or stenting [4]. Therapeutic strategies often involve the use of drug-eluting stents (DES) that release agents such as Sirolimus or Paclitaxel to locally inhibit these pathways and prevent vessel re-narrowing [2]. While these interventions are highly effective at reducing restenosis, they also pose risks such as delayed re-endothelialization and late stent thrombosis due to the non-selective inhibition of cell growth [4]. Consequently, these pathways are a major focus of cardiovascular research aimed at identifying more selective molecular targets that can distinguish between pathological and regenerative cell processes.

Other names

VSMC proliferationVascular smooth muscle cell growth pathwaysNeointimal hyperplasia pathwaysVascular remodeling pathways

Inhibition of intracellular signaling cascades, such as the mTOR pathway or microtubule assembly, to arrest the cell cycle and prevent excessive smooth muscle cell division in the vessel wall [2][4].