Department of Pharmacology, University of Arizona, Tucson, Arizona, USA.
Anesthesiology. 2011 Jul;115(1):189-204. doi: 10.1097/ALN.0b013e31821b1ac5.
Nerve growth factor (NGF) was originally discovered as a neurotrophic factor essential for the survival of sensory and sympathetic neurons during development. However, in the adult NGF has been found to play an important role in nociceptor sensitization after tissue injury. The authors outline mechanisms by which NGF activation of its cognate receptor, tropomyosin-related kinase A receptor, regulates a host of ion channels, receptors, and signaling molecules to enhance acute and chronic pain. The authors also document that peripherally restricted antagonism of NGF-tropomyosin-related kinase A receptor signaling is effective for controlling human pain while appearing to maintain normal nociceptor function. Understanding whether there are any unexpected adverse events and how humans may change their behavior and use of the injured/degenerating tissue after significant pain relief without sedation will be required to fully appreciate the patient populations that may benefit from these therapies targeting NGF.
神经生长因子（NGF）最初被发现是一种神经营养因子，对于发育过程中感觉神经元和交感神经元的存活至关重要。然而，在成年后，NGF 被发现对组织损伤后的伤害感受器敏化起着重要作用。作者概述了 NGF 与其同源受体原肌球蛋白相关激酶 A 受体的激活如何调节一系列离子通道、受体和信号分子，以增强急性和慢性疼痛。作者还记录到，外周限制 NGF-原肌球蛋白相关激酶 A 受体信号的拮抗作用对于控制人类疼痛是有效的，同时似乎维持了正常伤害感受器的功能。为了充分了解可能受益于这些靶向 NGF 治疗的患者群体，需要了解是否存在任何意外的不良反应，以及在没有镇静作用的情况下，人类在明显减轻疼痛后如何改变其对受损/退化组织的行为和使用。
