Research progress on ferroptosis mediated by microglia in hypoxic-ischemic brain damage.
- Author:
Tao GUO
1
;
Hanjun ZUO
2
;
Xianfeng KUANG
2
;
Shukun ZHANG
2
;
Bolin CHEN
2
;
Lixing LUO
2
;
Xiao YANG
3
;
Zhao WANG
2
;
Juanjuan LI
4
Author Information
1. Department 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.
2. Department of Human Anatomy and Embryology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China.
3. Department of Anatomy, School of Basic Medical Sciences, School of Medicine, Kunming University of Science and Technology, Kunming 650500, China.
4. Department of Human Anatomy and Embryology, School of Basic Medical Sciences, Kunming Medical University, Kunming 650500, China. *Corresponding author, E-mail: lijuanjuan@kmmu.edu.cn.
- Publication Type:English Abstract
- MeSH:
Microglia/physiology*;
Ferroptosis/physiology*;
Humans;
Animals;
Hypoxia-Ischemia, Brain/pathology*;
Signal Transduction
- From:
Chinese Journal of Cellular and Molecular Immunology
2025;41(6):552-558
- CountryChina
- Language:Chinese
-
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.
