Vascular Smooth Muscle Cell Migration and P70S6K: Key Players in Intimal Hyperplasia Development

[Background] Vascular smooth muscle cell (VSMC) recruitment and activation by vessel injury cause intimal hyperplasia (IH) and restenosis. Drug‐eluting stents releasing mTOR (mechanistic target of rapamycin) blockers (sirolimus, everolimus [EV]) improve surgery outcomes but exhibit nonspecific effec...

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Bibliographic Details
Authors: Moreno‐Estar, Sara, Cidad, Pilar, Arévalo-Martínez, Marycarmen, Portillo, Ana M., Sacristan‐Moraleda, Marcos, Alonso, Esperanza, López-López, José R.
Format: article
Status:Published version
Publication Date:2025
Country:España
Institution:Consejo Superior de Investigaciones Científicas (CSIC)
Repository:DIGITAL.CSIC. Repositorio Institucional del CSIC
OAI Identifier:oai:digital.csic.es:10261/400386
Online Access:http://hdl.handle.net/10261/400386
Access Level:Open access
Keyword:Everolimus
Intimal hyperplasia
Kv1.3 channel blockers
P70S6K
Vascular smooth muscle cell migration
Description
Summary:[Background] Vascular smooth muscle cell (VSMC) recruitment and activation by vessel injury cause intimal hyperplasia (IH) and restenosis. Drug‐eluting stents releasing mTOR (mechanistic target of rapamycin) blockers (sirolimus, everolimus [EV]) improve surgery outcomes but exhibit nonspecific effects and poor efficacy in diseased vessels. Drug combinations targeting the multifactorial processes leading to IH could enhance efficacy and reduce toxicity. Our previous work showed that Kv1.3 channel blockers such as 5‐(4‐phenoxybutoxy)psoralen (PAP‐1) prevented IH. Since Kv1.3 signaling works through the MEK/ERK pathway, we hypothesize that PAP‐1 and EV combination could improve antirestenotic therapies.

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