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Investigate the molecular role of hepatocyte long noncoding RNA Fendrr in driving interleukin-6 production and hepatic stellate cell activation during liver fibrosis progression.

May 16, 2024Journal of Biological ChemistryOpen Access

The increase of long noncoding RNA Fendrr in hepatocytes contributes to liver fibrosis by promoting IL-6 production

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Investigate the molecular role of hepatocyte long noncoding RNA Fendrr in driving interleukin-6 production and hepatic stellate cell activation during liver fibrosis progression.
Examined hepatic expression levels of long noncoding RNA Fendrr and interleukin-6 (IL-6) across patient fibrotic liver specimens.
Evaluated correlative associations among hepatocyte Fendrr levels, IL-6 expression, hepatic stellate cell (HSC) activation markers, and histological fibrosis severity.
Fendrr expression in patient liver tissue increased in positive correlation with both the severity of liver fibrosis and hepatic IL-6 expression.
Hepatic IL-6 expression correlated positively with the extent of liver fibrosis and markers of hepatic stellate cell activation.

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Implication

Translational study reveals elevated lncRNA Fendrr drives IL-6 production and stellate cell activation in fibrotic liver tissue, highlighting a potential therapeutic target.

Cite This Study

Kang et al. (2024) studied this question.

synapsesocial.com/papers/69fff2384716aad0cc858776 https://doi.org/10.1016/j.jbc.2024.107376

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Implication

Translational study reveals elevated lncRNA Fendrr drives IL-6 production and stellate cell activation in fibrotic liver tissue, highlighting a potential therapeutic target.

The increase of long noncoding RNA Fendrr in hepatocytes contributes to liver fibrosis by promoting IL-6 production

Key Points

Discussion

Implication

Cite This Study

The increase of long noncoding RNA Fendrr in hepatocytes contributes to liver fibrosis by promoting IL-6 production

Key Points

Discussion

Implication

Cite This Study

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