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首页> 外文期刊>Neuroscience Research: The Official Journal of the Japan Neuroscience Society >The role of angiogenic and wound-healing factors after spinal cord injury in mammals.
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The role of angiogenic and wound-healing factors after spinal cord injury in mammals.

机译:哺乳动物脊髓损伤后血管生成和伤口愈合因子的作用。

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摘要

Patients with spinal cord injury (SCI) are permanently paralysed and anaesthetic below the lesion. This morbidity is attributed to the deposition of a dense scar at the injury site, the cellular components of which secrete axon growth inhibitory ligands that prevent severed axons reconnecting with denervated targets. Another complication of SCI is wound cavitation where a fluid filled cyst forms in the peri-lesion neuropil, enlarging over the first few months after injury and causes secondary axonal damage. Wound healing after SCI is accompanied by angiogenesis, which is regulated by angiogenic proteins, produced in response to oxygen deprivation. Necrosis in and about the SCI lesion sites may be suppressed by promoting angiogenesis and the resulting neuropil protection will enhance recovery after SCI. This review addresses the use of angiogenic/wound-healing related proteins including vascular endothelial growth factor, fibroblast growth factor, angiopoietin-1, angiopoietin-2 and transforming growth factor-β to moderate necrosis and axon sparing after SCI, providing a conducive environment for growth essential to functional recovery.
机译:脊髓损伤(SCI)的患者在病变以下永久瘫痪和麻醉。这种发病率归因于损伤部位沉积致密瘢痕,其细胞组分分泌轴突生长抑制性配体,该配体防止断裂轴突与去除的靶标进行重新连接。 SCI的另一个并发症是伤口空化,其中在Peri-病病毒神经潜水中含有液体囊性囊肿,在损伤后的前几个月内扩大并导致次要轴突损伤。 SCI伴随血管生成后的伤口愈合,其由血管生成蛋白调节,响应于缺氧缺乏而产生。通过促进血管生成,可以抑制SCI病变位点的坏死,并且由此产生的神经潜入物保护将在SCI后提高恢复。本次审查涉及使用血管生成/伤口愈合相关蛋白质,包括血管内皮生长因子,成纤维细胞生长因子,血管发球子-1,血管发成素-2和转化在SCI之后的中等坏死和轴突中的增殖因子-β,提供有利于的环境对功能恢复至关重要的增长。

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