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Published on: March 15, 2024
FAdV-4-induced ferroptosis affects fat metabolism in LMH cells
Wenjing Dong1, Ke Du1, Yonghe Ding1
1The Affiliated Hospital of Qingdao University and The Biomedical Sciences Institute of Qingdao University (Qingdao Branch of SJTU Bio-X Institutes), Qingdao University, Qingdao, Shandong Province, China.
Abstract:
Ferroptosis is a form of controlled cell death that was first described relatively recently and that is dependent on the formation and accumulation of lipid free radicals through an iron-mediated mechanism. A growing body of evidence supports the close relationship between pathogenic infections and ferroptotic cell death, particularly for viral infections. Ferroptosis is also closely tied to the pathogenic development of hepatic steatosis and other forms of liver disease. Fowl adenovirus serotype 4 (FAdV-4) is a hepatotropic aviadenovirus causing hydropericardium syndrome (HPS) that is capable of impacting fat metabolism. However, it remains uncertain as to what role, if any, ferroptotic death plays in the context of FAdV-4 infection. Here, FAdV-4 was found to promote ferroptosis via the p53-SLC7A11-GPX4 axis, while ferrostain-1 was capable of inhibiting this FAdV-4-mediated ferroptotic death through marked reductions in lipid peroxidation. The incidence of FAdV-4-induced fatty liver was also found to be associated with the activation of ferroptotic activity. Together, these results offer novel insights regarding potential approaches to treating HPS.
Insights
Fowl adenovirus serotype 4 (FAdV-4) promotes ferroptosis, a cell death pathway, in liver cells. Inhibiting this process may offer new treatments for hydropericardium syndrome (HPS) and fatty liver disease.
Area of Science:
- Cell Biology
- Virology
- Pathology
Background:
- Ferroptosis is iron-dependent cell death involving lipid radical accumulation.
- Viral infections and liver diseases like fatty liver are linked to ferroptosis.
- Fowl adenovirus serotype 4 (FAdV-4) causes hydropericardium syndrome (HPS) and affects fat metabolism.
Purpose of the Study:
- To investigate the role of ferroptosis in FAdV-4 infection.
- To explore the molecular mechanisms of FAdV-4-induced ferroptosis.
- To assess the therapeutic potential of inhibiting ferroptosis in FAdV-4 infection.
Main Methods:
- FAdV-4 infection in cell models.
- Analysis of the p53-SLC7A11-GPX4 pathway.
- Assessment of lipid peroxidation.
- Administration of ferrostatin-1 (an inhibitor of ferroptosis).
- Evaluation of FAdV-4-induced fatty liver.
Main Results:
- FAdV-4 infection activates ferroptosis through the p53-SLC7A11-GPX4 axis.
- Ferrostatin-1 significantly reduces FAdV-4-mediated lipid peroxidation and cell death.
- FAdV-4-induced fatty liver is associated with increased ferroptotic activity.
Conclusions:
- FAdV-4 promotes ferroptosis via a specific molecular pathway.
- Inhibition of ferroptosis can mitigate FAdV-4-induced cell damage and fatty liver.
- Targeting ferroptosis presents a potential therapeutic strategy for HPS.
