Fiche du document
2022
- doi: 10.3389/fphys.2022.1081881
- issn: 1664-042X
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.3389/fphys.2022.1081881
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/36685215
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pissn/1664-042X
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_84BC9965E4A73
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
Sujets proches
Muscle, Vascular Blood-vessels--Muscles illnessCiter ce document
S. Déglise et al., « Vascular smooth muscle cells in intimal hyperplasia, an update. », Serveur académique Lausannois, ID : 10.3389/fphys.2022.1081881
Métriques
Partage / Export
Résumé
Arterial occlusive disease is the leading cause of death in Western countries. Core contemporary therapies for this disease include angioplasties, stents, endarterectomies and bypass surgery. However, these treatments suffer from high failure rates due to re-occlusive vascular wall adaptations and restenosis. Restenosis following vascular surgery is largely due to intimal hyperplasia. Intimal hyperplasia develops in response to vessel injury, leading to inflammation, vascular smooth muscle cells dedifferentiation, migration, proliferation and secretion of extra-cellular matrix into the vessel's innermost layer or intima. In this review, we describe the current state of knowledge on the origin and mechanisms underlying the dysregulated proliferation of vascular smooth muscle cells in intimal hyperplasia, and we present the new avenues of research targeting VSMC phenotype and proliferation.