Phenotypic Diversity of Vascular Smooth Muscle Cells in Pulmonary Arterial Hypertension: Implications for Therapy.
Fiche du document
- doi: 10.1016/j.chest.2021.08.040
- issn: 0012-3692
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.chest.2021.08.040
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/34391758
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/1931-3543
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_AAC3F5EFBCC12
info:eu-repo/semantics/openAccess , CC BY-NC-ND 4.0 , https://creativecommons.org/licenses/by-nc-nd/4.0/
Sujets proches
Phenotypes Muscle Musculature Myodynamics MyologyCiter ce document
B. Lechartier et al., « Phenotypic Diversity of Vascular Smooth Muscle Cells in Pulmonary Arterial Hypertension: Implications for Therapy. », Serveur académique Lausannois, ID : 10.1016/j.chest.2021.08.040
Métriques
Partage / Export
Résumé
Pulmonary arterial hypertension (PAH) is a progressive incurable condition that is characterized by extensive remodeling of the pulmonary circulation, leading to severe right-sided heart failure and death. Similar to other vascular contractile cells, pulmonary arterial smooth muscle cells play central roles in physiological and pathologic vascular remodeling because of their remarkable ability to dynamically modulate their phenotype to ensure contractile and synthetic functions. The dysfunction and molecular mechanisms underlying their contribution to the various pulmonary vascular lesions associated with PAH have been a major focus of research. The aim of this review is to describe the medial and nonmedial origins of contractile cells in the pulmonary vascular wall and present evidence of how they contribute to the onset and progression of PAH. We also highlight specific potential target molecules and discuss future directions that are being explored to widen the therapeutic options for the treatment of PAH.