Institute of Neurobiology, Medical Sciences Campus, University of Puerto Rico, 201 Blvd. del Valle, San Juan, PR, 00901, USA.
Mol Neurobiol. 2020 Jan;57(1):51-66. doi: 10.1007/s12035-019-01756-w. Epub 2019 Nov 7.
Injuries typically result in the development of neuropathic pain, which decreases in parallel with wound healing. However, the pain may remain after the injury appears to have healed, which is generally associated with an ongoing underlying pro-inflammatory state. Injury induces many cells to release factors that contribute to the development of a pro-inflammatory state, which is considered an essential first step towards wound healing. However, pain elimination requires a transition of the injury site from pro- to anti-inflammatory. Therefore, developing techniques that eliminate chronic pain require an understanding of the cells resident at and recruited to injury sites, the factors they release, that promote a pro-inflammatory state, and promote the subsequent transition of that site to be anti-inflammatory. Although a relatively large number of cells, factors, and gene expression changes are involved in these processes, it may be possible to control a relatively small number of them leading to the reduction and elimination of chronic neuropathic pain. This first of two papers examines the roles of the most salient cells and mediators associated with the development and maintenance of chronic neuropathic pain. The following paper examines the cells and mediators involved in reducing and eliminating chronic neuropathic pain.
损伤通常会导致神经性疼痛的发展，这种疼痛会随着伤口愈合而逐渐减轻。然而，在损伤似乎已经愈合后，疼痛可能仍然存在，这通常与持续存在的潜在炎症状态有关。损伤会诱导许多细胞释放有助于炎症状态发展的因素，这被认为是伤口愈合的重要第一步。然而，消除疼痛需要损伤部位从促炎状态向抗炎状态的转变。因此，开发消除慢性疼痛的技术需要了解驻留在损伤部位和募集到损伤部位的细胞、它们释放的促进促炎状态的因子，以及促进该部位随后向抗炎状态的转变。尽管这些过程涉及相对大量的细胞、因子和基因表达变化，但可能可以控制相对较少的细胞，从而减少和消除慢性神经性疼痛。这两篇论文中的第一篇探讨了与慢性神经性疼痛的发展和维持相关的最显著细胞和介质的作用。下一篇论文探讨了减少和消除慢性神经性疼痛所涉及的细胞和介质。
