Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death.
CCN2
CTGF
FoxD1
Hypoplasia
Lung
Skeletogenesis
Journal
Journal of cell communication and signaling
ISSN: 1873-9601
Titre abrégé: J Cell Commun Signal
Pays: Netherlands
ID NLM: 101308338
Informations de publication
Date de publication:
Mar 2020
Mar 2020
Historique:
pubmed:
16
4
2020
medline:
16
4
2020
entrez:
16
4
2020
Statut:
ppublish
Résumé
Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in for example kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2
Identifiants
pubmed: 32291573
doi: 10.1007/s12079-020-00559-2
pii: 10.1007/s12079-020-00559-2
pmc: PMC7176786
doi:
Types de publication
Published Erratum
Langues
eng
Pagination
47-52Commentaires et corrections
Type : ErratumFor
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