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Updated: Apr 21, 2026
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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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OSBPL2 deficiency alleviates diet-induced MASLD by reducing ACSL4-mediated ferroptosis.
Tianming Wang1,2, Fanghong Sheng3, Chao Lian1,2
1Central Laboratory, The Affiliated Jiangning Hospital with Nanjing Medical University, Nanjing, Jiangsu, China.
Iscience
|April 20, 2026
Summary
Oxysterol-binding protein-like 2 (OSBPL2) regulates lipid homeostasis and iron metabolism. OSBPL2 deficiency protects against ferroptosis and liver fibrosis, suggesting it
Area of Science:
- Biochemistry
- Cell Biology
- Hepatology
Background:
- Oxysterol-binding protein-like 2 (OSBPL2) impacts lipid homeostasis but its role in iron and fatty acid metabolism is unclear.
- Iron overload is linked to metabolic dysfunction-associated steatotic liver disease (MASLD) progression.
Purpose of the Study:
- To investigate the role of OSBPL2 in coordinating iron and fatty acid homeostasis.
- To explore OSBPL2's function in ferroptosis and diet-induced liver fibrosis.
Main Methods:
- Investigated OSBPL2 binding partners, including HSP90β.
- Assessed the impact of OSBPL2 deficiency on hepatic fatty acid metabolism, lipolysis, and ACSL4 expression.
- Evaluated ferroptosis resistance and liver fibrosis in OSBPL2-depleted mice.
Main Results:
- OSBPL2 interacts with HSP90β.
- OSBPL2 deficiency impairs lipolysis, alters hepatic fatty acid distribution, and inhibits ACSL4 expression.
- OSBPL2 depletion confers resistance to ferroptosis via the ACSL4 pathway and attenuates liver fibrosis in mice.
Conclusions:
- OSBPL2 plays a critical role in regulating iron and fatty acid homeostasis.
- OSBPL2 is implicated in ferroptosis and liver fibrosis progression.
- OSBPL2 represents a potential therapeutic target for MASLD.
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