IndraLab

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"USP14 overexpressing (pAd-USP14) mice exhibited increased diet-induced adipose tissue inflammation and pro-inflammatory cytokine secretion, which exacerbated IR."
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"Thus, this study describes a novel mechanism by which USP14 mediates chronic inflammation in adipose tissue and highlights USP14 inhibition as a key strategy to counteract this inflammatory response a[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Consistent with previous study, our study demonstrated that USP14 knockdown attenuated OGD/R treatment mediated the enhancement effect on SK-N-SH cell inflammation, apoptosis, and ferroptosis, indicating that USP14 accelerates the progression of stroke.Ferroptosis is a mechanism of cell death after ischemia in many organs, such as the kidney and heart."
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"Therefore, it would be interesting to investigate the role of USP14 in ER stress induced inflammation in IBD."
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"Our previous studies have revealed that USP14 increases cellular lipid peroxidation, inflammation, and fibrosis in the liver."
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"Further analysis indicated that TGT caused a significant inflammatory response in liver endothelial cells at different spatial locations; led to marked inflammatory response, apoptosis and fatty acid metabolism dysfunction in hepatocytes; activated hepatic stellate cells; brought about the activation, inflammation, and phagocytosis of liver capsular macrophages cells; resulted in immune dysfunction of liver lymphocytes; disturbed the intercellular crosstalk in liver microenvironment by regulating various signaling pathways."
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"Inhibition of USP14 suppresses ferroptosis and inflammation in LPS-induced goat mammary epithelial cells through ubiquitylating the IL-6 protein ."
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"TGT administration significantly increased the inflammatory response score compared to the control group (all P < 0.001, Figs."
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"Furthermore, TGT leads to the activation, inflammation, and phagocytosis processes in liver capsular macrophages, while also induces immune dysfunction within liver lymphocytes."
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"Moreover, the expression of several S100 isoforms (including S100a4, S100a6, S100a8, and S100a9) has increased pro-inflammatory and pro-fibrotic activities [20] in all endothelial cell subtypes under TGT stimulation.3.4 TGT treatment caused marked inflammatory response, apoptosis, and fatty acid metabolism dysfunction in hepatocytes."
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"Further analysis indicated that TGT treatment significantly increased the inflammatory response score (Figs."
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"In contrast to the control group, we discovered that TGT treatment significantly increased reactive oxygen species (ROS) scores and inflammatory response scores in both qHSC and aHSC subtypes (Figs."
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"In summary, the TGT treatment led to the activation, inflammation, and phagocytosis of LCM cells.3.7 TGT treatment caused the immune dysfunction of liver lymphocytes."
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"Hepatic USP14 overexpression exacerbated diet-induced hepatic steatosis, inflammation and fibrosis in mice, in contrast to the results of hepatic USP14 knockdown."
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"Furthermore, palmitic/oleic acid-induced lipid peroxidation and inflammation in hepatocytes were markedly increased by USP14 overexpression but decreased by USP14 knockdown."
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"Ubiquitin specific protease 14 (USP14) contributes the progress of inflammation associated diseases."
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"Moreover, TGT increased the inflammatory response scores and EMT scores markedly."
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"USP14 promotes hepatic LPO and inflammation by increasing CYP2E1."
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"GA could mitigate TGT-induced acute liver injury by mediating PKM2, reducing oxidative stress and inflammation and reducing hepatocyte apoptosis."
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"However, its role in the mastitis was little known.In this experiment, using LPS stimulated goat mammary epithelial cells (GMECs) as an in vitro inflammation model, we study the effects and mechanism of IL-6 and USP14 on LPS-induced GMEC inflammation and ferroptosis."
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"Previous research has demonstrated that hepatic USP14 expression is much higher in NAFLD patients and that hepatic USP14 overexpression exacerbates diet-induced hepatic steatosis, inflammation, and fibrosis in mice, in contrast to the results of hepatic USP14 knockdown (107, 108)."
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"In DR patients, USP14 can modulate inflammatory response through the TGF-β1 signal transduction, IκBα and NF-κB signaling pathway s in HG-treated Müller cells, as well as reactive oxygen species (ROS) (126)."
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"Our study found increased expression of hepatic USP14 with the development of NAFLD, which directly led to an increase of CYP2E1, inducing more severe ROS, mitochondrial damage, and inflammation."
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