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Extracellular Vesicles in Pathogenesis and Treatment of Metabolic Associated Fatty Liver Disease
Ji Sun1, Dianbao Zhang2, Yiling Li1
1Department of Gastroenterology, The First Affiliated Hospital of China Medical University, Shenyang, China.
Abstract:
Metabolic associated fatty liver disease (MAFLD) is the most common chronic liver disease worldwide due to the sedentary and overeating lifestyle. Yet, the pathophysiology of MAFLD is still unclear and no drug has been approved for MAFLD treatment. Extracellular vesicles (EVs) are heterogenous membrane-bound particles released from almost all types of cells. These nano-sized particles mediate intercellular communication through their bioactive cargos including nucleic acids, proteins, and lipids. The EVs modulate metabolic homeostasis via communication between adipose tissue and liver. The dysregulation of lipid metabolism leads to inflammation in liver and the number and compounds of EVs are changed during MAFLD. The injured hepatocytes secrete EVs to induce the migration of bone marrow-derived monocytes and the activation of macrophages in liver. The EVs secreted by different cells regulate the alteration of hepatic stellate cell (HSC) phenotypes and HSC activation gives rise to liver fibrosis. Based on the participation of EVs in MAFLD progression, we discuss the prospects of EVs as a therapeutic target and their application in drug delivery.
Insights
Metabolic associated fatty liver disease (MAFLD) involves changes in extracellular vesicles (EVs). EVs play a role in MAFLD progression, offering potential as therapeutic targets and for drug delivery.
Area of Science:
- Hepatology
- Cell Biology
- Biochemistry
Background:
- Metabolic associated fatty liver disease (MAFLD) is a prevalent global liver condition linked to lifestyle factors.
- The precise mechanisms driving MAFLD pathophysiology remain incompletely understood, with no approved pharmacological treatments.
- Extracellular vesicles (EVs), nanoscale particles mediating intercellular communication, are implicated in metabolic homeostasis between adipose tissue and the liver.
Purpose of the Study:
- To explore the role of extracellular vesicles (EVs) in the progression of Metabolic associated fatty liver disease (MAFLD).
- To discuss the potential of EVs as therapeutic targets for MAFLD.
- To evaluate the application of EVs in drug delivery strategies for MAFLD.
Main Methods:
- Literature review on the involvement of EVs in MAFLD pathogenesis.
- Analysis of EV composition and function in the context of altered lipid metabolism and liver inflammation.
- Examination of EV-mediated interactions between hepatocytes, immune cells, and hepatic stellate cells.
Main Results:
- Dysregulated lipid metabolism in MAFLD alters the quantity and content of EVs.
- EVs from injured hepatocytes promote monocyte migration and macrophage activation in the liver.
- EVs influence hepatic stellate cell phenotype and activation, contributing to liver fibrosis.
Conclusions:
- EVs are integral to MAFLD progression, participating in inflammation and fibrosis.
- Targeting EVs presents a promising therapeutic avenue for MAFLD.
- EVs hold potential as a drug delivery system for MAFLD treatment.
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