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Cell Autophagy in NASH and NASH-Related Hepatocellular Carcinoma
Utibe-Abasi S Udoh1,2, Pradeep Kumar Rajan1,2, Yuto Nakafuku1,2
1Department of Surgery, Marshall University Joan C. Edwards School of Medicine, Huntington, WV 25701, USA.
Abstract:
Autophagy, a cellular self-digestion process, involves the degradation of targeted cell components such as damaged organelles, unfolded proteins, and intracellular pathogens by lysosomes. It is a major quality control system of the cell and plays an important role in cell differentiation, survival, development, and homeostasis. Alterations in the cell autophagic machinery have been implicated in several disease conditions, including neurodegeneration, autoimmunity, cancer, infection, inflammatory diseases, and aging. In non-alcoholic fatty liver disease, including its inflammatory form, non-alcoholic steatohepatitis (NASH), a decrease in cell autophagic activity, has been implicated in the initial development and progression of steatosis to NASH and hepatocellular carcinoma (HCC). We present an overview of autophagy as it occurs in mammalian cells with an insight into the emerging understanding of the role of autophagy in NASH and NASH-related HCC.
Insights
Autophagy, a cellular process, is crucial for maintaining cell health. Impaired autophagy contributes to non-alcoholic steatohepatitis (NASH) and liver cancer development.
Area of Science:
- Cell Biology
- Molecular Biology
- Gastroenterology
Background:
- Autophagy is a fundamental cellular process for degrading damaged components and maintaining homeostasis.
- Dysregulation of autophagy is linked to various diseases, including neurodegeneration, cancer, and aging.
- Reduced autophagic activity is implicated in the progression of non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH) and hepatocellular carcinoma (HCC).
Purpose of the Study:
- To provide an overview of mammalian autophagy.
- To explore the role of autophagy in the pathogenesis of NASH.
- To discuss the involvement of autophagy in NASH-related HCC.
Main Methods:
- Literature review of autophagy mechanisms.
- Analysis of studies investigating autophagy in NAFLD and NASH.
- Synthesis of current research on autophagy's role in HCC development.
Main Results:
- Autophagy acts as a critical cellular quality control mechanism.
- Decreased autophagy promotes steatosis and inflammation in the liver, driving NASH progression.
- Autophagy modulation is a potential therapeutic target for NASH and HCC.
Conclusions:
- Autophagy plays a significant role in liver homeostasis and disease.
- Understanding autophagy's function in NASH is vital for developing targeted therapies.
- Further research into autophagy pathways could lead to novel treatments for liver diseases.
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