Author Correction: Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitis

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Author Correction: Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitis

Summary of https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9918510/

  • Alcoholic hepatitis (AH) is a severe form of alcoholic liver disease (ALD) characterized by inflammation and necrosis of the liver.
  • Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in the regulation of hepatic gene expression.
  • In this study, the authors investigated the role of HNF4α in the pathogenesis of AH.
  • They found that HNF4α expression was significantly decreased in AH patients compared to healthy controls.
  • They also found that HNF4α-dependent gene expression was significantly decreased in AH patients.
  • The authors concluded that defective HNF4α-dependent gene expression is a driver of hepatocellular failure in AH.

Detailed Summary

Alcoholic hepatitis (AH) is a severe form of alcoholic liver disease (ALD) characterized by inflammation and necrosis of the liver. It is a major cause of morbidity and mortality in patients with ALD, and is associated with a high risk of mortality. Despite its clinical importance, the molecular mechanisms underlying AH remain poorly understood.

Hepatocyte nuclear factor 4 alpha (HNF4α) is a transcription factor that plays a critical role in the regulation of hepatic gene expression. It is known to be involved in the regulation of genes involved in lipid metabolism, glucose homeostasis, and inflammation. However, its role in the pathogenesis of AH has not been investigated.

In this study, the authors investigated the role of HNF4α in the pathogenesis of AH. They analyzed the expression of HNF4α in liver tissue samples from AH patients and healthy controls. They found that HNF4α expression was significantly decreased in AH patients compared to healthy controls.

The authors then investigated the effect of HNF4α on gene expression in AH patients. They found that HNF4α-dependent gene expression was significantly decreased in AH patients. This suggests that defective HNF4α-dependent gene expression is a driver of hepatocellular failure in AH.

The authors concluded that defective HNF4α-dependent gene expression is a driver of hepatocellular failure in AH. This finding provides new insights into the molecular mechanisms underlying AH and may lead to the development of new therapeutic strategies for the treatment of this disease.

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