CCN3 (NOV) Drives Degradative Changes in Aging Articular Cartilage.
Animals
Cartilage, Articular
/ growth & development
Cell Line, Tumor
Cells, Cultured
Cellular Senescence
Chondrocytes
/ metabolism
Cyclin-Dependent Kinase Inhibitor p21
/ genetics
Humans
Mice
Mice, Inbred C57BL
Nephroblastoma Overexpressed Protein
/ genetics
Osteoarthritis, Knee
/ metabolism
Rats
Tumor Suppressor Protein p53
/ genetics
CCN3
NOV
SASP
aging
cellular communication network factor 3
oxidative stress
p21
p53
primary chondrocytes
senescence
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:
13 Oct 2020
13 Oct 2020
Historique:
received:
04
09
2020
revised:
06
10
2020
accepted:
08
10
2020
entrez:
17
10
2020
pubmed:
18
10
2020
medline:
26
2
2021
Statut:
epublish
Résumé
Aging is a major risk factor of osteoarthritis, which is characterized by the degeneration of articular cartilage. CCN3, a member of the CCN family, is expressed in cartilage and has various physiological functions during chondrocyte development, differentiation, and regeneration. Here, we examine the role of CCN3 in cartilage maintenance. During aging, the expression of
Identifiants
pubmed: 33066270
pii: ijms21207556
doi: 10.3390/ijms21207556
pmc: PMC7593953
pii:
doi:
Substances chimiques
Ccn3 protein, mouse
0
Cyclin-Dependent Kinase Inhibitor p21
0
Nephroblastoma Overexpressed Protein
0
Trp53 protein, mouse
0
Tumor Suppressor Protein p53
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : JSPS KAKENHI
ID : 16K11476
Organisme : JSPS KAKENHI
ID : 25462888
Organisme : JSPS KAKENHI
ID : 20K18601
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