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STING-mediated inflammation contributes to Gao binge ethanol feeding model
Ling Wang1, Hong-Mei You1, Hong-Wu Meng1
1Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Institute of Innovative Drugs, School of Pharmacy, Anhui Medical University, Hefei, China.
Journal of Cellular Physiology
|October 26, 2021
Summary
Alcohol metabolism releases mitochondrial DNA (mtDNA), triggering inflammation. STING acts as an mtDNA sensor, worsening liver injury and hepatocyte apoptosis in alcoholic liver disease models.
Area of Science:
- Hepatology and immunology
- Molecular and cellular biology
Background:
- Alcohol metabolism induces liver injury through hepatocyte damage-associated molecular patterns (DAMPs).
- Mitochondrial DNA (mtDNA) released from damaged hepatocytes promotes inflammation.
- STING, a DAMPs pattern recognition receptor, is implicated in innate immunity but its role in alcoholic liver injury is unclear.
Purpose of the Study:
- To investigate the expression and function of STING in the Gao binge ethanol model of alcoholic liver injury.
- To elucidate the role of STING as an mtDNA sensor in liver inflammation and hepatocyte apoptosis.
Main Methods:
- Utilized the Gao binge ethanol model to study alcoholic liver injury.
- Examined STING upregulation and its signaling pathway.
- Investigated STING's role as an mtDNA sensor in Kupffer cells.
Main Results:
- STING expression was significantly upregulated in the Gao binge ethanol model.
- STING functions as an mtDNA sensor in liver Kupffer cells.
- STING activation leads to inflammation and exacerbates hepatocyte apoptosis.
Conclusions:
- STING signaling pathway activation contributes to alcoholic liver injury.
- STING acts as a key mediator linking mtDNA release to inflammation and apoptosis.
- Targeting STING may offer a therapeutic strategy for alcoholic liver disease.
