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Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
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DCN released from ferroptotic cells ignites AGER-dependent immune responses
Jiao Liu1, Shan Zhu2, Ling Zeng3
1Center for DAMP Biology, Third Affiliated Hospital of Guangzhou Medical University, Guangdong, China.
Autophagy
|December 29, 2021
Summary
Decorin (DCN) released during ferroptosis acts as an alarm signal, activating immune responses via the DCN-AGER pathway. Inhibiting this axis protects against pancreatitis and limits tumor immunity.
Area of Science:
- Cell Biology
- Immunology
- Biochemistry
Background:
- Ferroptosis is a regulated cell death pathway implicated in inflammation.
- Key mediators initiating immune responses during ferroptosis are largely unknown.
Purpose of the Study:
- To identify mediators released during ferroptosis that trigger immune responses.
- To elucidate the mechanism by which ferroptosis signals to the immune system.
Main Methods:
- Analysis of proteins released by ferroptotic cells.
- Investigating the role of decorin (DCN) in immune activation.
- Utilizing pharmacological and genetic inhibition of the DCN-advanced glycosylation end-product-specific receptor (AGER) axis.
- Assessing effects in models of acute pancreatitis and cancer.
Main Results:
- Decorin (DCN) is actively released during ferroptosis via secretory autophagy and lysosomal exocytosis.
- Extracellular DCN binds to the receptor AGER on macrophages, inducing pro-inflammatory cytokine production dependent on NF-κB signaling.
- Inhibition of the DCN-AGER axis ameliorates ferroptosis-induced acute pancreatitis and reduces the tumor-protective immune response.
Conclusions:
- Decorin (DCN) functions as a critical alarm signal mediating the inflammatory and immune consequences of ferroptosis.
- The DCN-AGER axis represents a potential therapeutic target for ferroptosis-related inflammatory diseases and cancer immunotherapy.
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