Publications by authors named "Yin-Cui Wu"

Nonalcoholic fatty liver disease (NAFLD) is one of the common causes of chronic liver disease in the world. The problem of NAFLD had become increasingly prominent. However, its pathogenesis is still indistinct.

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Article Synopsis
  • Non-alcoholic fatty liver disease (NAFLD) is a widespread health issue linked to obesity and insulin resistance, characterized by excessive triglyceride buildup in the liver, leading to inflammation and cell damage.
  • This study explored the role of P38γ, a protein that influences inflammation, using both in vivo and in vitro experiments to assess its impact on NAFLD in mice and liver cells.
  • The findings revealed that higher P38γ levels are associated with increased liver damage; reducing P38γ expression significantly lessened liver injury and lipid accumulation, indicating its potential as a therapeutic target for managing fatty liver disease.
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Common liver tissue damage is mainly due to the accumulation of toxic aldehydes in lipid peroxidation under oxidative stress. Cumulative toxic aldehydes in the liver can be effectively metabolized by acetaldehyde dehydrogenase 2 (ALDH2), thereby alleviating various liver diseases. Notably, gene mutation of ALDH2 leads to impaired ALDH2 enzyme activity, thus aggravating the progress of liver diseases.

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Acetaminophen (APAP) is one of the major causes of drug-induced acute liver injury, and ethanol may aggravate APAP-induced liver injury. The problem of ethanol- and APAP-induced liver injury becomes increasingly prominent, but the mechanism of ethanol- and APAP-induced liver injury remains ambiguous. p38γ is one of the four isoforms of P38 mitogen activated protein kinases, that contributes to inflammation in different diseases.

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