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Updated: May 24, 2025

A Model for Encephalomyosynangiosis Treatment after Middle Cerebral Artery Occlusion-Induced Stroke in Mice
Published on: June 22, 2022
Imatinib on target in stroke recovery
Abstract:
Ischemic stroke causes scars in the CNS that impede functional recovery, and there is a need for therapeutics to improve recovery after the acute phase. Scar-resident myofibroblasts and the PDGF pathway have been implicated in stroke pathology. In this issue of the JCI, Protzmann et al. report that inhibition of PDGF-CC or its receptor, PDGFRα, reduces the myofibroblast population and improves functional recovery after ischemic stroke in mice. Importantly, PDGFRα inhibition was effective in improving functional recovery even when initiated 24 hours after stroke, which suggests opportunities for later treatment by targeting the PDGF pathway. This study demonstrates the therapeutic potential of enhancing stroke recovery even after acute damage and blood-brain barrier dysfunction has already occurred.
Insights
Targeting the PDGF pathway after ischemic stroke in mice reduced scarring and improved functional recovery, even when treatment began 24 hours post-stroke. This highlights potential for later-phase stroke therapeutics.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Pharmacology
Background:
- Ischemic stroke leads to central nervous system (CNS) scarring that hinders functional recovery.
- Myofibroblasts and the platelet-derived growth factor (PDGF) pathway are implicated in stroke pathology.
- There is a critical need for therapeutics to enhance recovery after the acute phase of stroke.
Purpose of the Study:
- To investigate the therapeutic potential of inhibiting the PDGF pathway for improving functional recovery after ischemic stroke.
- To determine if targeting PDGF-CC or its receptor PDGFRα can reduce scar formation and enhance recovery.
Main Methods:
- The study utilized a mouse model of ischemic stroke.
- Inhibition of PDGF-CC or its receptor, PDGFRα, was administered.
- Functional recovery and myofibroblast populations were assessed post-treatment.
Main Results:
- Inhibition of PDGF-CC or PDGFRα significantly reduced the myofibroblast population in the stroke scar.
- PDGFRα inhibition led to improved functional recovery in mice after ischemic stroke.
- Therapeutic effects were observed even when PDGFRα inhibition was initiated 24 hours after stroke.
Conclusions:
- Targeting the PDGF pathway, specifically PDGFRα, holds therapeutic potential for enhancing functional recovery after ischemic stroke.
- Inhibition of PDGFRα is effective even when initiated in the later phase after stroke, suggesting a viable treatment window beyond the acute phase.
- This research opens avenues for developing novel therapeutics to improve long-term outcomes for stroke survivors by addressing scar-mediated recovery deficits.
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