About this Research Topic
Acute axonal injury in the central nervous system (CNS) such as following stroke, brain or spinal cord trauma, results in axonal degeneration, lack of regeneration and long-term neurological disability due to the dysfunction of neuronal networks. In fact, damaged CNS axons not only degenerate but are especially unable to regenerate and have a limited capacity to sprout and re-establish lost connections.
The reasons for this deficient axonal regeneration are the presence of a glial inhibitory environment that induces growth cone collapse and the lack of the intrinsic capacity of injured neurons to mount a pro-regenerative gene expression response.
At the core of the intrinsic neuronal gene expression potential is the cellular transcriptional machinery, formed by transcription factors and co-factors together with the epigenetic modifications (epigenetic marks) that contribute to the overall transcriptional control. In the last several years, it has been shown how the modulation of transcription via specific genetic or pharmacological manipulation can be instrumental to promote axonal regeneration in rodents in a number of peripheral and CNS axonal injury models.
This Research Topic issue aims to provide a platform for scientists in the field to critically discuss past and recent experimental evidence about the role of transcription in axonal outgrowth and regeneration. In addition, it welcomes novel contributions that would improve our understanding of the intrinsic properties of neurons that shape their pro-regenerative gene expression properties in response to axonal injuries.
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.