Abstract
Central nervous system (CNS) injury, including stroke, spinal cord injury, and traumatic brain injury, causes severe neurological symptoms such as sensory and motor deficits. Currently, there is no effective therapeutic method to restore neurological function because the adult CNS has limited capacity to regenerate after injury. Many efforts have been made to understand the molecular and cellular mechanisms underlying CNS regeneration and to establish novel therapeutic methods based on these mechanisms, with a variety of strategies including cell transplantation, modulation of cell intrinsic molecular mechanisms, and therapeutic targeting of the pathological nature of the extracellular environment in CNS injury. In this review, we will focus on the mechanisms that regulate CNS regeneration, highlighting the history, recent efforts, and questions left unanswered in this field.
Highlights
Damage to the central nervous system (CNS), such as in stroke, spinal cord injury (SCI), and traumatic brain injury, leads to severe neurological dysfunction due to neuronal cell death and axonal degeneration
Recent advances in high-throughput technologies utilized in transcriptomics, proteomics, genomics, and cellular imaging have accelerated the identification of novel molecular mechanisms as a therapeutic target that effectively regulates axon growth, regeneration, and remyelination, and promotes functional recovery after CNS injury
Olig1-cre mice were crossed with RiboTag mice [72] to generate mice expressing HA-tagged ribosomal protein in oligodendrocyte lineage cells (OLCs). These mice were fed with a cuprizone diet for 9 weeks, and OLC-specific ribosome-associated mRNAs were isolated from the corpus callosum with or without 3 weeks of remyelination with a normal diet
Summary
Damage to the central nervous system (CNS), such as in stroke, spinal cord injury (SCI), and traumatic brain injury, leads to severe neurological dysfunction due to neuronal cell death and axonal degeneration. Emerging evidence has suggested that cell intrinsic mechanisms in adult CNS neurons play an important role in the regenerative process after injury [3]. Considering that spontaneous axon regeneration is slightly observed in several non-primate and primate animal models of CNS injury [4,5] and is considered to contribute to partially restoring locomotor function, it should be worth focusing on cell intrinsic mechanisms of CNS axon regeneration to promote this process. In addition to axonal regeneration, remyelination is an important regenerative process to restore lost neurological function [6]. Recent advances in high-throughput technologies utilized in transcriptomics, proteomics, genomics, and cellular imaging have accelerated the identification of novel molecular mechanisms as a therapeutic target that effectively regulates axon growth, regeneration, and remyelination, and promotes functional recovery after CNS injury.
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