Hypoxia Inducible Factor 1A Supports a Pro-Fibrotic Phenotype Loop in Idiopathic Pulmonary Fibrosis.
HIF1A
IPF
PAI-1
bleomycin
extracellular matrix
fibrosis
in-vivo
nintedanib
signaling
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
24 Mar 2021
24 Mar 2021
Historique:
received:
03
03
2021
revised:
18
03
2021
accepted:
22
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
10
6
2021
Statut:
epublish
Résumé
Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with poor prognosis. The IPF-conditioned matrix (IPF-CM) system enables the study of matrix-fibroblast interplay. While effective at slowing fibrosis, nintedanib has limitations and the mechanism is not fully elucidated. In the current work, we explored the underlying signaling pathways and characterized nintedanib involvement in the IPF-CM fibrotic process. Results were validated using IPF patient samples and bleomycin-treated animals with/without oral and inhaled nintedanib. IPF-derived primary human lung fibroblasts (HLFs) were cultured on Matrigel and then cleared using NH
Identifiants
pubmed: 33805152
pii: ijms22073331
doi: 10.3390/ijms22073331
pmc: PMC8078165
pii:
doi:
Substances chimiques
HIF1A protein, human
0
Hif1a protein, rat
0
Hypoxia-Inducible Factor 1, alpha Subunit
0
Indoles
0
Bleomycin
11056-06-7
nintedanib
G6HRD2P839
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
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