Nuclear receptor subfamily 1 group D member 1 suppresses the proliferation, migration of adventitial fibroblasts, and vascular intimal hyperplasia via mammalian target of rapamycin complex 1/β-catenin pathway.
beta Catenin
/ metabolism
Cell Movement
Cell Proliferation
Cells, Cultured
Fibroblasts
Hyperplasia
/ metabolism
Ki-67 Antigen
/ metabolism
Mechanistic Target of Rapamycin Complex 1
/ metabolism
Muscle, Smooth, Vascular
Myocytes, Smooth Muscle
Neointima
/ genetics
Nuclear Receptor Subfamily 1, Group D, Member 1
/ metabolism
TOR Serine-Threonine Kinases
/ metabolism
AFs
NR1D1
mTORC1
neointimal hyperplasia
β-catenin
Journal
Clinical and experimental hypertension (New York, N.Y. : 1993)
ISSN: 1525-6006
Titre abrégé: Clin Exp Hypertens
Pays: England
ID NLM: 9305929
Informations de publication
Date de publication:
31 Dec 2023
31 Dec 2023
Historique:
entrez:
16
2
2023
pubmed:
17
2
2023
medline:
18
2
2023
Statut:
ppublish
Résumé
In-stent restenosis hardly limits the therapeutic effect of the percutaneous vascular intervention. Although the restenosis is significantly ameliorated after the application of new drug-eluting stents, the incidence of restenosis remains at a high level. Vascular adventitial fibroblasts (AFs) play an important role in intimal hyperplasia and subsequent restenosis. The current study was aimed to investigate the role of nuclear receptor subfamily 1, group D, member 1 (NR1D1) in the vascular intimal hyperplasia. We observed increased expression of NR1D1 after the transduction of adenovirus carrying These data suggest that NR1D1 inhibits intimal hyperplasia by suppressing the proliferation and migration of AFs in a mTORC1/β-catenin-dependent manner.
Sections du résumé
BACKGROUND
UNASSIGNED
In-stent restenosis hardly limits the therapeutic effect of the percutaneous vascular intervention. Although the restenosis is significantly ameliorated after the application of new drug-eluting stents, the incidence of restenosis remains at a high level.
OBJECTIVE
UNASSIGNED
Vascular adventitial fibroblasts (AFs) play an important role in intimal hyperplasia and subsequent restenosis. The current study was aimed to investigate the role of nuclear receptor subfamily 1, group D, member 1 (NR1D1) in the vascular intimal hyperplasia.
METHODS AND RESULTS
UNASSIGNED
We observed increased expression of NR1D1 after the transduction of adenovirus carrying
CONCLUSION
UNASSIGNED
These data suggest that NR1D1 inhibits intimal hyperplasia by suppressing the proliferation and migration of AFs in a mTORC1/β-catenin-dependent manner.
Identifiants
pubmed: 36794491
doi: 10.1080/10641963.2023.2178659
doi:
Substances chimiques
beta Catenin
0
Ki-67 Antigen
0
Mechanistic Target of Rapamycin Complex 1
EC 2.7.11.1
Nuclear Receptor Subfamily 1, Group D, Member 1
0
SR9009
0
TOR Serine-Threonine Kinases
EC 2.7.11.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM