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MAFLD: a ferroptotic disease
1College of Biomedicine and Health, College of Life Science and Technology, Huazhong Agricultural University, Wuhan, Hubei 430070, China.
Abstract:
Ferroptosis, a regulated cell death pathway driven by iron-catalyzed lipid peroxidation, has recently been implicated as a major cause of hepatic injury in metabolic dysfunction-associated fatty liver disease (MAFLD). This review highlights how the identification of hyperoxidized peroxiredoxin 3 (PRDX3) as a ferroptosis-specific marker has led to the discovery that ferroptosis contributes to liver injury in MAFLD, and summarizes other emerging evidence connecting ferroptosis to MAFLD pathogenesis. These new findings suggest that dietary fat composition and genetic variants such as PNPLA3(I148M) may affect the progression of MAFLD by regulating cellular sensitivity to ferroptosis. Recognizing MAFLD as a ferroptotic disease provides novel insights into the pathogenesis of the disease, and supports the exploration of ferroptosis as a potential target for therapeutic intervention.
Insights
Ferroptosis, a cell death pathway, significantly contributes to liver injury in metabolic dysfunction-associated fatty liver disease (MAFLD). Targeting ferroptosis offers a promising therapeutic strategy for MAFLD.
Area of Science:
- Biochemistry
- Cell Biology
- Hepatology
Background:
- Metabolic dysfunction-associated fatty liver disease (MAFLD) is a growing health concern.
- Hepatic injury is a key feature of MAFLD pathogenesis.
- Ferroptosis, an iron-dependent cell death, is increasingly recognized in liver diseases.
Purpose of the Study:
- To review the role of ferroptosis in MAFLD.
- To highlight ferroptosis as a driver of liver injury in MAFLD.
- To explore ferroptosis as a therapeutic target for MAFLD.
Main Methods:
- Literature review of ferroptosis and MAFLD.
- Analysis of ferroptosis-specific markers, such as hyperoxidized peroxiredoxin 3 (PRDX3).
- Examination of genetic and dietary factors influencing ferroptosis in MAFLD.
Main Results:
- Ferroptosis, marked by PRDX3, is a significant contributor to liver injury in MAFLD.
- Emerging evidence links ferroptosis to MAFLD pathogenesis.
- Dietary fat and genetic variants (e.g., PNPLA3(I148M)) modulate ferroptosis sensitivity in MAFLD.
Conclusions:
- MAFLD can be viewed as a ferroptotic disease.
- Understanding ferroptosis in MAFLD provides novel pathogenetic insights.
- Ferroptosis inhibition is a potential therapeutic avenue for MAFLD.
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