Sodium thiosulfate acts as a hydrogen sulfide mimetic to prevent intimal hyperplasia via inhibition of tubulin polymerisation.
Hydrogen sulfide
Intimal hyperplasia
Proliferation
Smooth muscle cells
Sodium thiosulfate
Journal
EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039
Informations de publication
Date de publication:
Apr 2022
Apr 2022
Historique:
received:
09
08
2021
revised:
08
03
2022
accepted:
08
03
2022
pubmed:
26
3
2022
medline:
27
4
2022
entrez:
25
3
2022
Statut:
ppublish
Résumé
Intimal hyperplasia (IH) remains a major limitation in the long-term success of any type of revascularisation. IH is due to vascular smooth muscle cell (VSMC) dedifferentiation, proliferation and migration. The gasotransmitter Hydrogen Sulfide (H Low density lipoprotein receptor deleted (LDLR STS inhibited IH in WT mice, as well as in LDLR STS, a drug used for the treatment of cyanide poisoning and calciphylaxis, protects against IH in a mouse model of arterial restenosis and in human vein segments. STS acts as an H This work was supported by the Swiss National Science Foundation (grant FN-310030_176158 to FA and SD and PZ00P3-185927 to AL); the Novartis Foundation to FA; and the Union des Sociétés Suisses des Maladies Vasculaires to SD, and the Fondation pour la recherche en chirurgie vasculaire et thoracique.
Sections du résumé
BACKGROUND
BACKGROUND
Intimal hyperplasia (IH) remains a major limitation in the long-term success of any type of revascularisation. IH is due to vascular smooth muscle cell (VSMC) dedifferentiation, proliferation and migration. The gasotransmitter Hydrogen Sulfide (H
METHODS
METHODS
Low density lipoprotein receptor deleted (LDLR
FINDINGS
RESULTS
STS inhibited IH in WT mice, as well as in LDLR
INTERPRETATION
CONCLUSIONS
STS, a drug used for the treatment of cyanide poisoning and calciphylaxis, protects against IH in a mouse model of arterial restenosis and in human vein segments. STS acts as an H
FUNDING
BACKGROUND
This work was supported by the Swiss National Science Foundation (grant FN-310030_176158 to FA and SD and PZ00P3-185927 to AL); the Novartis Foundation to FA; and the Union des Sociétés Suisses des Maladies Vasculaires to SD, and the Fondation pour la recherche en chirurgie vasculaire et thoracique.
Identifiants
pubmed: 35334307
pii: S2352-3964(22)00138-4
doi: 10.1016/j.ebiom.2022.103954
pmc: PMC8941337
pii:
doi:
Substances chimiques
Thiosulfates
0
Tubulin
0
Cystathionine gamma-Lyase
EC 4.4.1.1
sodium thiosulfate
HX1032V43M
Hydrogen Sulfide
YY9FVM7NSN
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
103954Informations de copyright
Copyright © 2022 The Author(s). Published by Elsevier B.V. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no competing interests.