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Evaluating Cell Death Signaling by Immunofluorescence in a Rat Model of Ischemic Stroke
Published on: January 3, 2025
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Microglial Autophagy and Mitophagy in Ischemic Stroke: From Dual Roles to Therapeutic Modulation.
Juan Wu1, Jiaxin Liu1, Yanwen Li1
1Medical School, Kunming University of Science and Technology, Kunming 650500, China.
Biology
|September 27, 2025
Summary
Microglial autophagy and mitophagy play dual roles in ischemic stroke. Modulating these processes shows therapeutic potential for stroke, but human studies and biomarkers are needed.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Ischemic stroke triggers complex neuroinflammation.
- Microglial autophagy and mitophagy have dual roles in stroke injury and repair.
Purpose of the Study:
- To review evidence on microglial autophagy and mitophagy mechanisms in ischemic stroke.
- To explore their therapeutic implications for stroke treatment.
Main Methods:
- Scoping review of literature from PubMed and Embase.
- Included 39 original research articles and 13 reviews.
- Search terms: microglia, autophagy, ischemic stroke.
Main Results:
- Protective autophagy linked to AMPK activation, mTOR inhibition, and mitophagy pathways (PINK1/Parkin, BNIP3/NIX).
- Therapeutic agents (rapamycin, Tat-Beclin 1, Urolithin A) showed neuroprotection in preclinical models.
- Excessive autophagy associated with inflammasome activation and oxidative stress.
Conclusions:
- Phase-specific modulation of microglial autophagy is a potential therapeutic strategy for stroke.
- Further validation in human models and development of autophagy biomarkers are necessary for clinical application.

