Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury.
Implications of enolase in the RANKL-mediated osteoclast activity following spinal cord injury.
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DOI：
10.32604/biocell.2021.017659
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发表时间：
2021-09-01
期刊：
影响因子：
--
通讯作者：
Haque A
中科院分区：
文献类型：
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作者：
Shams R;Banik NL;Haque A
脊髓损伤（SCI）是一种以脊髓损伤为特征的衰弱性疾病，导致功能、活动性和感觉丧失。虽然在美国越来越普遍，但由于病情的不幸复杂性，没有FDA批准的治疗方法，SCI的困难可能会因SCI相关并发症（如骨质疏松症）的发展而进一步加剧。SCI展示了两个关键的考虑阶段：初级阶段和次级阶段。虽然初级阶段被认为是即时的和不可逆的，但次级阶段被认为是治疗干预的一个有希望的机会窗口。烯醇化酶是一种在SCI后上调的代谢酶，它执行非糖酵解功能，通过细胞外降解作用促进炎症事件，并增加炎症细胞因子和趋化因子的产生。神经元特异性烯醇化酶（NSE）是脊髓损伤后神经元功能损伤的生物标志物，抑制NSE可减轻脊髓损伤后继发性损伤，改善功能障碍。这篇观点文章涉及到RANK-RANKL通路调控中的烯醇化酶激活，并简要总结了SCI中破骨细胞介导的骨吸收的影响机制。我们的实验室提出，抑制烯醇化酶的激活可能会减少SCI诱导的炎症反应，降低破骨细胞的活性，限制SCI中骨骼组织丢失的机会。
Spinal Cord Injury (SCI) is a debilitating condition characterized by damage to the spinal cord, resulting in loss of function, mobility, and sensation. Although increasingly prevalent in the US, no FDA-approved therapy exists due to the unfortunate complexity of the condition, and the difficulties of SCI may be furthered by the development of SCI-related complications, such as osteoporosis. SCI demonstrates two crucial stages for consideration: the primary stage and the secondary stage. While the primary stage is suggested to be immediate and irreversible, the secondary stage is proposed as a promising window of opportunity for therapeutic intervention. Enolase, a metabolic enzyme upregulated after SCI, performs non-glycolytic functions, promoting inflammatory events via extracellular degradative actions and increased production of inflammatory cytokines and chemokines. Neuron-specific enolase (NSE) serves as a biomarker of functional damage to neurons following SCI, and the inhibition of NSE has been demonstrated to reduce signs of secondary injury of SCI and to ameliorate dysfunction. This Viewpoint article involves enolase activation in the regulation of RANK-RANKL pathway and summarizes succinctly the mechanisms influencing osteoclast-mediated resorption of bone in SCI. Our laboratory proposes that inhibition of enolase activation may reduce SCI-induced inflammatory response and decrease osteoclast activity, limiting the chances of skeletal tissue loss in SCI.