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Updated: Sep 19, 2025
Author Spotlight: Tracing the Ferroptotic Signatures and Cell Death Dynamics in Medulloblastoma for Advanced Therapeutics
Published on: March 15, 2024
[Research progress on ferroptosis mediated by microglia in hypoxic-ischemic brain damage]
Tao Guo1, Hanjun Zuo2, Xianfeng Kuang2
1Department of Human Anatomy and Embryology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500; Department of Anatomy, School of Basic Medical Sciences, School of Medicine, Kunming University of Science and Technology, Kunming 650500, China.
Abstract:
In hypoxic-ischemic brain damage (HIBD), the programmed cell death known as ferroptosis is significantly activated. Microglial cells demonstrate a high level of sensitivity to iron accumulation. Understanding how to regulate the dual role of microglia and transforming the microglial ferroptosis to a moderate and controllable process has considerable implications for the targeted treatment in HIBD. This paper serves as an overview of microglia-mediated ferroptosis in HIBD as a disease model. We discuss various aspects centered around microglia, including pathophysiological mechanisms, polarization and functions of microglia, molecular mechanisms of ferroptosis, signaling pathways, and therapeutic strategies. The review aims to provide a reference for studies of ferroptosis in microglia.
Insights
Ferroptosis, a cell death pathway, is activated in hypoxic-ischemic brain damage (HIBD). Targeting microglial ferroptosis offers a potential therapeutic strategy for HIBD.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Hypoxic-ischemic brain damage (HIBD) involves significant ferroptosis activation.
- Microglial cells are highly sensitive to iron accumulation, a key factor in ferroptosis.
- Regulating microglial ferroptosis is crucial for HIBD treatment.
Purpose of the Study:
- To provide an overview of microglia-mediated ferroptosis in HIBD.
- To discuss the pathophysiological mechanisms, polarization, and functions of microglia in HIBD.
- To explore molecular mechanisms, signaling pathways, and therapeutic strategies for ferroptosis in microglia.
Main Methods:
- Literature review and synthesis of existing research on microglia and ferroptosis in HIBD.
- Analysis of pathophysiological mechanisms and molecular pathways involved.
- Discussion of therapeutic interventions targeting microglial ferroptosis.
Main Results:
- Microglia play a dual role in HIBD, with their ferroptosis being a significant contributor.
- Understanding microglial ferroptosis mechanisms is key to developing targeted HIBD therapies.
- Various signaling pathways and molecular targets are implicated in microglial ferroptosis.
Conclusions:
- Microglia-mediated ferroptosis is a critical process in HIBD.
- Modulating microglial ferroptosis presents a promising therapeutic avenue for HIBD.
- This review serves as a reference for future research on ferroptosis in microglia within the HIBD context.
