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.