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Updated: Jun 4, 2025
Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
Adipocyte-derived ferroptotic signaling mitigates obesity
Xue Wang1, Qian Wu2, Meijuan Zhong3
1The Second Affiliated Hospital, School of Public Health, State Key Laboratory of Experimental Hematology, Zhejiang University School of Medicine, Hangzhou 310058, China; The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Hangzhou 310058, China; School of Public Health, Basic Medical Sciences, School of Pharmacology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang 421001, China; School of Public Health, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China.
Activating ferroptosis, an iron-dependent cell death, in adipose tissue reduces lipid accumulation and combats obesity. This process involves key proteins and pathways, offering potential therapeutic strategies for metabolic disorders.
Area of Science:
- Cell Biology
- Metabolic Disorders
- Biochemistry
Background:
- Ferroptosis is an iron-dependent form of cell death.
- The role of ferroptosis in adipose tissue remains largely unknown.
- Obesity is linked to altered adipose tissue function.
Purpose of the Study:
- To investigate the role of ferroptosis in adipose tissue.
- To explore ferroptosis as a therapeutic target for obesity and metabolic disorders.
Main Methods:
- Analysis of ferroptotic signatures in adipose tissue from obese individuals and mice.
- Treatment of primary adipocytes and high-fat diet-fed mice with ferroptosis agonists.
- Genetic manipulation: overexpression of Acsl4 and deletion of Fth in adipocytes.
- Mechanistic studies involving 5,15-DiHETE, HIF1α, c-Myc, and Pgc1β.
Main Results:
- Obese individuals and mice exhibit a reduced ferroptotic signature in adipose tissue.
- Activation of ferroptosis signaling decreases lipid accumulation in adipocytes and ameliorates HFD-induced obesity.
- Acsl4 overexpression or Fth deletion protects against HFD-induced adipose expansion and metabolic dysfunction.
- 5,15-DiHETE activates ferroptosis, degrades HIF1α, and derepresses a thermogenic program via the c-Myc-Pgc1β pathway.
Conclusions:
- Ferroptosis signaling is suppressed in obesity.
- Activating ferroptosis in adipose tissue can reduce lipid accumulation and improve metabolic health.
- Targeting ferroptosis pathways presents a potential strategy for preventing and treating obesity and related metabolic disorders.
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