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Sustaining microglial reparative function enhances stroke recovery
Jun Tsuyama1,2,3, Seiichiro Sakai4,5,6, Kumiko Kurabayashi4,5,6
1Department of Neuroinflammation and Repair, Medical Research Laboratory, Institute of Science Tokyo, Tokyo, Japan. tsuyama.j.662a@m.isct.ac.jp.
Nature
|May 13, 2026
Summary
Researchers found that ZFP384 causes microglia to lose their beneficial functions after a stroke. Targeting ZFP384 can restore these functions and improve brain recovery, even long after the injury.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Neurological deficits after brain injury often persist due to diminished spontaneous recovery.
- Microglia play a critical role in brain repair, but the mechanisms limiting recovery are not fully understood.
Purpose of the Study:
- To investigate the cellular and molecular mechanisms behind the loss of microglial reparative functions post-stroke.
- To identify therapeutic targets for enhancing long-term brain functional recovery.
Main Methods:
- Cellular fate analysis was employed to track microglial function after stroke.
- Investigated the role of the transcriptional regulator ZFP384 in microglial dysfunction.
- Utilized antisense oligonucleotides targeting Zfp384 in preclinical models.
Main Results:
- Reparative microglia persist post-stroke but lose beneficial functions.
- ZFP384 was identified as a key regulator diminishing reparative gene expression in microglia.
- ZFP384 inhibits YY1-mediated chromatin interactions essential for repair gene induction.
- Targeting Zfp384 with antisense oligonucleotides sustained microglial repair functions and improved chronic stroke recovery.
Conclusions:
- ZFP384-mediated microglial dysfunction contributes to limited functional recovery after stroke.
- Therapeutic strategies targeting ZFP384 can restore microglial reparative immunity and promote prolonged brain repair.
- Preventing the loss of immune cell restorative functions offers a promising approach for enhancing neurological recovery.
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