|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Taken together, our results showed that broussonin E could suppress inflammation by modulating macrophages activation statevia inhibiting the ERK and p38 MAPK and enhancing JAK2-STAT3 signaling pathway, and can be further developed as a promising drug for the treatment of inflammation-related diseases such as atherosclerosis.
|
31171272 |
2019 |
|
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
IL-8 interacted with its receptor CXC chemokine receptor 2 (CXCR2) on neutrophils, leading to the formation of NETs via Src and extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinases (MAPK) signaling to aggravate AS progression <i>in vivo</i>.
|
31496351 |
2019 |
|
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Influence of crocetin on high-cholesterol diet induced atherosclerosis in rats via anti-oxidant activity together with inhibition of inflammatory response and p38 MAPK signaling pathway.
|
29692651 |
2018 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways, thereby achieved its anti-adipogenic effect, anti-oxidant effect and anti-inflammation effect in a dose-dependent manner in AS.
|
29793330 |
2018 |
|
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Systemic inflammation associated with COPD, is often hypothesised as a causal factor. p38 mitogen-activated protein kinases play a key role in the inflammatory pathogenesis of COPD and atherosclerosis.
|
29566026 |
2018 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Effects of Tianxiangdan Granule treatment on atherosclerosis via NF‑κB and p38 MAPK signaling pathways.
|
29257205 |
2018 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
This review summarizes experimental findings relating to p38 MAPK in atherosclerosis and aortic valve sclerosis and discusses potential functions of p38 MAPK in the diseases with the aim of clarifying its eligibility as a pharmacological target.
|
30486366 |
2018 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
The most promising anti-inflammatory compounds for treatment of atherosclerosis include non-specific anti-inflammatory drugs, phospholipase inhibitors, blockers of major inflammatory cytokines, leukotrienes, adhesion molecules, and pro-inflammatory signaling pathways, such as CCL2-CCR2 axis or p38 MAPK pathway.
|
29378168 |
2018 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
In conclusion, LEE suppresses LPS-induced upregulation of inflammatory factors, adhesion molecules and MCP-1 in rat VSMCs mainly via inhibiting the p38 MAPK/NF-κB pathways, thus partly uncovered LEE's molecular mechanisms for its therapeutic effect on atherosclerosis.
|
27592629 |
2017 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of a key signaling molecule of the p38 MAPK pathway, p38α MAPK/MAPK14, by selective inhibitors like skepinone-L, conclusively facilitates elucidation of the impact of the complex network of p38 MAPK signaling on atherogenesis and might provide a promising therapeutic tool to prevent inflammatory cascades in atherosclerosis.-Cheng, F., Twardowski, L., Fehr, S., Aner, C., Schaeffeler, E., Joos, T., Knorpp, T., Dorweiler, B., Laufer, S., Schwab, M., Torzewski, M. Selective p38α MAP kinase/MAPK14 inhibition in enzymatically modified LDL-stimulated human monocytes: implications for atherosclerosis.
|
27871059 |
2017 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
Factors implicated in the development of atherosclerosis including modified low-density lipoprotein (LDL), cytokines and even shear stress induce p38 activation in endothelial cells and macrophages, which may be important for plaque formation.
|
21695272 |
2011 |
|
Atherosclerosis
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Together, these results indicate that the glucose suppression of SR-B1 expression is partially mediated by the activation of the p38 MAPK-Sp1 pathway and raise the possibility that the inhibition of hepatic SR-BI expression under high-glucose conditions provides a mechanism for accelerated atherosclerosis in diabetics.
|
17957039 |
2008 |
|
Atherosclerosis
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results provide that acrolein may play a role in progression of atherosclerosis and new information on the signaling pathways involved in COX-2 upregulation in response to acrolein and provide evidence that PKCdelta and p38 MAPK are required for transcriptional activation of COX-2.
|
17363696 |
2007 |