探索神经病理性疼痛中血管生成的分子途径及其治疗意义。

Exploring the molecular pathways and therapeutic implications of angiogenesis in neuropathic pain.

作者信息

Sharma Aditi, Behl Tapan, Sharma Lalit, Shah Om Prakash, Yadav Shivam, Sachdeva Monika, Rashid Summya, Bungau Simona Gabriela, Bustea Cristiana

机构信息

School of Pharmaceutical Sciences, Shoolini University, Solan 173211, Himachal Pradesh, India.

School of Health Sciences and Technology, University of Petroleum and Energy Studies, Bidholi, 248007 Dehradun, Uttarakhand, India.

出版信息

Biomed Pharmacother. 2023 Jun;162:114693. doi: 10.1016/j.biopha.2023.114693. Epub 2023 Apr 14.

Abstract

Recently, much attention has been paid to chronic neuro-inflammatory condition underlying neuropathic pain. It is generally linked with thermal hyperalgesia and tactile allodynia. It results due to injury or infection in the nervous system. The neuropathic pain spectrum covers a variety of pathophysiological states, mostly involved are ischemic injury viral infections associated neuropathies, chemotherapy-induced peripheral neuropathies, autoimmune disorders, traumatic origin, hereditary neuropathies, inflammatory disorders, and channelopathies. In CNS, angiogenesis is evident in inflammation of neurons and pain in bone cancer. The role of chemokines and cytokines is dualistic; their aggressive secretion produces detrimental effects, leading to neuropathic pain. However, whether the angiogenesis contributes and exists in neuropathic pain remains doubtful. In the present review, we elucidated summary of diverse mechanisms of neuropathic pain associated with angiogenesis. Moreover, an overview of multiple targets that have provided insights on the VEGF signaling, signaling through Tie-1 and Tie-2 receptor, erythropoietin pathway promoting axonal growth are also discussed. Because angiogenesis as a result of these signaling, results in inflammation, we focused on the mechanisms of neuropathic pain. These factors are mainly responsible for the activation of post-traumatic regeneration of the PNS and CNS. Furthermore, we also reviewed synthetic and herbal treatments targeting angiogenesis in neuropathic pain.

摘要

最近,慢性神经炎症状态作为神经性疼痛的潜在病因已备受关注。它通常与热痛觉过敏和触觉异常性疼痛有关。其起因是神经系统的损伤或感染。神经性疼痛谱涵盖多种病理生理状态,其中主要涉及缺血性损伤、病毒感染相关神经病、化疗引起的周围神经病、自身免疫性疾病、创伤性病因、遗传性神经病、炎症性疾病以及离子通道病。在中枢神经系统中,血管生成在神经元炎症和骨癌疼痛中较为明显。趋化因子和细胞因子的作用具有双重性;它们的大量分泌会产生有害影响,导致神经性疼痛。然而,血管生成是否在神经性疼痛中起作用以及是否存在仍存在疑问。在本综述中,我们阐述了与血管生成相关的神经性疼痛的多种机制概述。此外,还讨论了多个靶点的概况,这些靶点为血管内皮生长因子(VEGF)信号传导、通过Tie-1和Tie-2受体的信号传导以及促红细胞生成素促进轴突生长的途径提供了见解。由于这些信号传导导致的血管生成会引发炎症,我们重点关注了神经性疼痛的机制。这些因素主要负责外周神经系统和中枢神经系统创伤后再生的激活。此外,我们还综述了针对神经性疼痛中血管生成的合成治疗和草药治疗。

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