Related Experiment Video
Updated: May 5, 2026
13:28
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
11.9K
From Tim4 to ischemic stroke: a mitochondrial pathway driving microglial M1 polarization
Zhinan Ye1, Yingying Jin2, Hao Xu1
1Department of Neurology, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University, Taizhou, China.
Brain Research
|January 3, 2026
Summary
T-cell immunoglobulin and mucin domain 4 (Tim4) promotes M1 microglial polarization and mitochondrial dysfunction in ischemic stroke. Targeting Tim4 offers a potential therapeutic strategy for stroke by modulating microglial responses.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia dysfunction is a key factor in ischemic stroke pathology.
- T-cell immunoglobulin and mucin domain 4 (Tim4) is implicated in microglial function.
Purpose of the Study:
- To investigate the role of Tim4 in microglial polarization and mitochondrial dynamics following ischemic stroke.
- To evaluate Tim4 as a potential therapeutic target for ischemic stroke.
Main Methods:
- Ischemic stroke was modeled using middle cerebral artery occlusion (MCAO) and oxygen-glucose deprivation (OGD) in rodents.
- Assessed infarct volume, neurological deficits, apoptosis, microglial polarization (M1/M2), Tim4 expression, mitochondrial fission proteins (MFF, Drp1), mitochondrial membrane potential (MMP), and reactive oxygen species (ROS).
Main Results:
- MCAO induced increased infarct volume, neurological deficits, apoptosis, and M1 microglia.
- Tim4 upregulation correlated with increased ROS, enhanced mitochondrial fission (MFF, Drp1), and reduced MMP in microglia.
- Tim4 knockdown reversed these effects, while Drp1 overexpression partially offset Tim4 knockdown's impact on microglial polarization.
Conclusions:
- Tim4 promotes M1 microglial polarization and mitochondrial fission in ischemic stroke.
- Tim4 regulates microglial M1 polarization through mitochondrial pathways.
- Tim4 represents a potential therapeutic target for treating ischemic stroke.
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