Summary Stroke remains a global health concern and a leading cause of adult-onset disability due to limited intrinsic repair capability. Here, we identify nucleolin as a targetable regulator of the repair programs activated following ischemic injury. Through neuron-specific subcellular targeting of axonal nucleolin in the post-stroke recovery period, we see enhanced axonal sprouting and accelerated functional recovery following motor cortex stroke. These findings demonstrate that interference in localized nucleolin functions following cortical stroke is a viable strategy to enhance functional recovery.
Bridges et al. (Mon,) studied this question.