脊髓损伤
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Figure 1｜Main factors hindering axon regeneration after spinal cord injury.
In most cases, spinal cord injury (SCI) leads to a series of functional impairment and psychological complications, which can be a disaster for patients, their families, and society (Hearn et al., 2018; Wang et al., 2018). It has been reported that more than 20 million people worldwide are affected by SCI, which often leaves them unable to take care of themselves (James et al., 2019), In the United States alone, there are 400,000 patients with SCI, with an additional 14,000 cases each year (Sekhon et al., 2001). After SCI, patients usually suffer from motor and sensory loss in the lower or upper extremities, and can have difficulty urinating and having sex (Ali et al., 2020; Moussa et al., 2020), which may need nursing and rehabilitation for the remainder of their life. Furthermore, most patients with SCI experience severe psychological problems due to neuropathic pain or other functional impairments (Shiao et al., 2018). While there is a clear need for an effective therapeutic strategy, the hunt has been long and the results generally disappointing, which has been attributed to several reasons (Figure 1).
Figure 2｜Post-translational modifications affect growth cone regeneration after spinal cord injury.
During nerve regeneration following SCI, there is significant neurite outgrowth and growth cone guidance, which can be identified by microtubule polymerization and de-polymerization. Microtubules are mainly composed of α-tubulin and β-tubulin. When the microtubules of neurons respond to physiological conditions, they can be modulated by PTMs. PTMs modify tubulin, which in turn modifies the physiological activities of microtubule functions (Janke et al., 2020). In the context of SCI, several PTMs have been reported to occur on tubulin, including phosphorylation (Atashi et al., 1992; Lang et al., 2015; Brandt et al., 2019), acetylation, detyrosination, and polyglutamylation, as shown in Figure 2.