|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
S-nitrosoglutathione attenuates the severity of LPS-induced AKI by inhibiting the TLR4-NF-κB signalling pathway and may act as a protective agent for septic AKI.
|
31115903 |
2019 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Mechanistic studies on modulation of AKI by Loganetin were performed using HK-2 cells and Toll-like receptor 4 (TLR4) knockout mice.
|
30706443 |
2019 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our study underscores an adaptive mechanism whereby TLR4 regulates SCF<sup>Fbxw7α</sup>-dependent Fn14 stabilization during inflammatory tubular damage and further supports investigation of targeting Fn14 in clinical trials of patients with septic AKI.
|
31017010 |
2019 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Harmine mitigates LPS-induced acute kidney injury through inhibition of the TLR4-NF-κB/NLRP3 inflammasome signalling pathway in mice.
|
30716318 |
2019 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
It was possible that MIF may mediate AKI via CD74/TLR4-NF-κB signalling as mice lacking MIF were protected from AKI by largely suppressing CD74/TLR-4-NF-κB associated renal inflammation, including the expression of MCP-1, TNF-α, IL-1β, IL-6, iNOS, CXCL15(IL-8 in human) and infiltration of macrophages, neutrophil, and T cells.
|
30968541 |
2019 |
|
Kidney Failure, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Acute kidney injury (AKI), a common complication of Gram-negative bacterial sepsis, is caused by Toll-like receptor 4 (TLR4) activation.
|
30915370 |
2019 |
|
Kidney Failure, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Valsartan prevents glycerol-induced acute kidney injury in male albino rats by downregulating TLR4 and NF-κB expression.
|
30053391 |
2018 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Hence, the present study aimed to evaluate the specific participation of TLR2 and TLR4 molecules on the development of cisplatin-induced AKI.
|
29500224 |
2018 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
CTD_human |
Relevance of megalin receptor injury with nuclear factor-kappa B upregulation in acute kidney injury induced in rats.
|
29286200 |
2018 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
TAK-242 did not reduce dysfunction and histological injury in the glycerol model of heme protein-induced acute kidney injury (AKI), findings corroborated by studies in TLR4<sup>+/+</sup> and TLR4<sup>-/-</sup> mice.
|
28978536 |
2018 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
These results show that DC-SIGN and TLR-4 interactions regulate inflammatory responses in renal tubular epithelial cells and participate in AKI pathogenesis.
|
28898406 |
2018 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
After contrast agent injection, the Scr and BUN levels of the experimental control group were significantly increased, the different doses applied in the atorvastatin group significantly reduced the Scr and BUN levels (p < .05) and ameliorated the contrast-induced acute kidney injury (p < .05) and significantly reduced Toll-like receptor 4 (TLR4), Myeloid differentiation factor 88 (Myd88), and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) protein expression and relative mRNA expression levels (p < .05) and significantly decreased expression levels of downstream inflammatory factors (p < .05).
|
28805489 |
2017 |
|
Kidney Failure, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The genes whose expression discriminated septic AKI from non-AKI included Toll like receptor 4 (up-regulated 2.7-fold, P = 0.04); Cyclooxygenase-2 (up-regulated 14.6-fold, P = 0.01), Angiotensin II Receptor (up-regulated 8.1-fold, P = 0.01), Caspase 3 (up-regulated 5.1-fold, P = 0.02), Peroxisome Proliferator-Activated Receptor Gamma, Coactivator 1 Alpha (down-regulated 2-fold, P = 0.02).
|
28569136 |
2017 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
From a physiological standpoint, inhibiting TLR4 in large animal experimental SI-AKI significantly improves renal function.
|
27602552 |
2017 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Our results demonstrated that the IL-18Rα-mediated signaling pathway plays critical roles in CD4⁺ T cells and APCs and responded more quickly to IFN-γ and IL-18 than TLR4 stimulation in the pathogenesis of LPS-induced AKI.
|
29261164 |
2017 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
This study investigated the possible renoprotective effect of telluric acid (TEL) against lipopolysaccharide (LPS)-induced acute kidney injury (AKI) in mice, targeting toll-like receptor 4 (TLR4), phosphoinositide 3-kinase (PI3K)/Akt, and nuclear factor-erythroid 2-related factor-2 (Nrf2) pathways as possible mechanistic contributors to TEL's effect.AKI was induced by LPS (2 mg/kg).TEL (60 μg/kg; i.p.) was administered once daily for seven consecutive days before LPS injection.
|
28685413 |
2017 |
|
Kidney Failure, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Targeting the HMGB1-TLR4 pathway might enable development of a new therapeutic strategy to improve the outcomes of severely ill patients with both acute lung and acute kidney injury.
|
24646859 |
2014 |