What mechanism does paclitaxel employ to decrease the incidence of restenosis in a stent?

Paclitaxel is a chemotherapeutic agent primarily known for its ability to inhibit cell division by stabilizing microtubules, thus preventing the normal breakdown of the mitotic spindle during cell division. When it comes to its use in stents, paclitaxel plays a critical role in reducing restenosis, which is the re-narrowing of an artery after it has been treated with a stent.

The primary mechanism by which paclitaxel decreases the incidence of restenosis is through the inhibition of smooth muscle cell proliferation over the stent. Following a stent implantation, the natural healing response of the vascular tissue includes migration and proliferation of smooth muscle cells. This process can lead to neointimal hyperplasia, which is the thickening of the vessel wall due to excessive growth of these cells, ultimately causing the artery to narrow again.

By utilizing paclitaxel, which disrupts the cycle of cell division, the growth of smooth muscle cells in the vicinity of the stent is significantly reduced, leading to a lower likelihood of restenosis. This targeted approach helps maintain the patency of the artery and improves the overall outcomes for patients receiving stented interventions.