|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study verified TXC's efficacy to treat OA in vivo and in vitro and suggests that p38 MAPK pathway-related mechanisms may be involved in TXC's therapeutic effects.
|
31760158 |
2020 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
After suppressing the p38 pathway, the chondrogenesis can be inhibited, which can be used to guide the treatment of osteoarthritis.
|
31831024 |
2019 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
(2) Can the P38 agonist anisomycin (ANS) induce mouse OA?
|
31308631 |
2019 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, β4GalT1 enhanced the ERK, JNK, and P38 MAPK signaling pathways through the induction of autocrine TNF-α signaling in OA-FLS.
|
31210280 |
2019 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Nanocrystals of a potent p38 MAPK inhibitor embedded in microparticles: Therapeutic effects in inflammatory and mechanistic murine models of osteoarthritis.
|
29524442 |
2018 |
|
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
More importantly, our results clearly demonstrated that the inhibitory effect of geniposide on surgery-induced expression of inflammatory mediators in osteoarthritis was closely associated with the suppression of the p38 MAPK signaling pathways.
|
29682561 |
2018 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, the results indicated that downregulated HS6ST2 targeted by miR-23b-3p promotes matrix degradation by activating p38 MAPK in chondrocytes and OA cartilage.
|
29899528 |
2018 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Cultured chondrocytes isolated from human OA cartilage were assigned into the blank group, the IL-1β group, the PD (PD980959, ERK pathway inhibitors)+IL-1β group, the SB (SB203580, p38 pathway inhibitors)+IL-1β group, and the SP (SP600125, JNK signaling pathway inhibitors)+IL-1β group.
|
27907835 |
2017 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our experimental results suggested that PDK1 may promote chondrocyte apoptosis in OA via p38 MAPK signaling pathway.
|
29061447 |
2017 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our results suggested that VPS4B might facilitate chondrocyte apoptosis in OA via p38 MAPK signaling pathway.
|
28744712 |
2017 |
|
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
So NR4A1 is likely to facilitate OA chondrocyte apoptosis, which is associated with p38 MAPK and mitochondrial apoptosis pathway.
|
28337303 |
2017 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
To reveal the mechanism and the effect of JNK and p38 MAPKs on matrix metalloproteinase 3 (MMP3) and autophagy in OA, the study established OA model in rabbits, used the measurement of the Osteoarthritis Research Society International scoring system to evaluate OA model, and conducted general observation, histological observation, and Western blotting of JNK, phosphorylate-JNK (P-JNK), p38, phosphorylate-p38 (P-p38), MMP3, and light-chain 3 (LC3)-II/LC3-I to explore the variation of JNK, p38 MAPKs, and autophagy at the early stage of OA.
|
26873249 |
2016 |
|
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our results showed that increased basal COL10A1 expression in OA hMSCs was significantly suppressed in the presence of JNK and p38 inhibitors, whereas Naproxen-induced COL10A1 expression was suppressed by 5-lipoxygenase inhibitor.
|
25091567 |
2015 |
|
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
OA and normal chondrocytes expressed p38; however, OA chondrocytes showed much higher phosphorylated p38 compared to normal chondrocytes.
|
21181091 |
2011 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The ERK-1/2 pathway inhibitor PD98059 significantly attenuated the hypertrophic changes induced by conditioned medium from OA SBOs, and the p38 inhibitor SB203580 resulted in the up-regulation of hypertrophic genes in ACCs.
|
20155832 |
2010 |
|
Degenerative polyarthritis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
These data suggest that BCP crystal induction of MMP-13 expression may involve the ERK1/2 and p38 MAPK pathways and activation of nuclear factor kappaB; this upregulation of MMP-13 may contribute to the accelerated cartilage breakdown in BCP crystal-associated osteoarthritis.
|
18223264 |
2008 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
We conclude that transamidation by TG2 transforms S100A11 into a covalently bonded homodimer that acquires the capacity to signal through the p38 MAPK pathway, accelerate chondrocyte hypertrophy and matrix catabolism, and thereby couple inflammation with chondrocyte activation to potentially promote OA progression.
|
18523305 |
2008 |
|
Degenerative polyarthritis
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study documents, for the first time, functional consequences of PAR-2 activation in human OA cartilage, identifies p38 as the major signalling pathway regulating its synthesis, and demonstrates that specific PAR-2 activation induces Erk1/2 and p38 in OA chondrocytes.
|
18031579 |
2007 |