IndraLab

Statements



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"In conclusion, these results indicate that USP29 knockout accelerates hepatic steatosis, inflammation and fibrosis induced by a HFHC diet."

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"Intriguingly, USP29 overexpression obviously attenuated hepatic steatosis, inflammation, collagen deposition and liver injury (Supplementary Fig. 4H–K)."

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"Thus, our results suggest that USP29 attenuates hepatic I/R injury by inhibiting the inflammatory response and apoptosis.We performed an RNA-sequencing (RNA-Seq) analysis of liver tissues from USP29 knockout mice and controls with I/R injury after 3h, and the results of the KEGG signaling pathway enrichment analysis showed that the MAPK signaling pathway was the most affected after USP29 knockout."

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"Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression."

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"The above results suggest that USP29 deficiency promotes local inflammation and hepatocyte apoptosis to exacerbate hepatic I/R injury."

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"USP29 overexpression inhibits hepatic injury, inflammatory response, and apoptosis."

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"USP29 knockout accelerates hepatic steatosis, inflammation and fibrosis induced by a HFHC diet."

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"Specifically, diet-induced hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression."