Protein post-translational modifications after spinal cord injury

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From: Neural Regeneration Research(Vol. 16, Issue 10)
Publisher: Medknow Publications and Media Pvt. Ltd.
Document Type: Report
Length: 8,850 words
Lexile Measure: 1440L

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Byline: Shuang. Zhu, Bing-Sheng. Yang, Si-Jing. Li, Ge. Tong, Jian-Ye. Tan, Guo-Feng. Wu, Lin. Li, Guo-Li. Chen, Qian. Chen, Li-Jun. Lin

Deficits in intrinsic neuronal capacities in the spinal cord, a lack of growth support, and suppression of axonal outgrowth by inhibitory molecules mean that spinal cord injury almost always has devastating consequences. As such, one of the primary targets for the treatment of spinal cord injury is to develop strategies to antagonize extrinsic or intrinsic axonal growth-inhibitory factors or enhance the factors that support axonal growth. Among these factors, a series of individual protein level disorders have been identified during the generation of axons following spinal cord injury. Moreover, an increasing number of studies have indicated that post-translational modifications of these proteins have important implications for axonal growth. Some researchers have discovered a variety of post-translational modifications after spinal cord injury, such as tyrosination, acetylation, and phosphorylation. In this review, we reviewed the post-translational modifications for axonal growth, functional recovery, and neuropathic pain after spinal cord injury, a better understanding of which may elucidate the dynamic change of spinal cord injury-related molecules and facilitate the development of a new therapeutic strategy for spinal cord injury.

Introduction

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 1}

Generally, SCI can be divided into three phases (Tator et al., 2009). The acute phase, which is caused by mechanical damage to spinal cord tissues from direct impact or shock waves, sets in motion a number of parallel pathophysiological processes. The mechanical disruption to neural and vascular tissue can lead to necrosis and cell death, and the ionic imbalance of K+, Na+, Ca2+ can lead to neural function impairment and spinal shock (Baumann, 2020). Furthermore, the severed axons undergo Wallerian degeneration of the distal part of the axon, as well as their associated myelin sheaths. The secondary stage (subacute injury phase) of SCI can occur anything from a few minutes to a few weeks after injury, during which the nervous...

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Gale Document Number: GALE|A652951276