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本文引用的文献

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Estrogen facilitates spinal cord synaptic transmission via membrane-bound estrogen receptors: implications for pain hypersensitivity.雌激素通过膜结合雌激素受体促进脊髓突触传递:对痛觉过敏的影响。
J Biol Chem. 2012 Sep 28;287(40):33268-81. doi: 10.1074/jbc.M112.368142. Epub 2012 Aug 6.
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Mechanisms of G protein-coupled estrogen receptor-mediated spinal nociception.G 蛋白偶联雌激素受体介导的脊髓伤害感受机制。
J Pain. 2012 Aug;13(8):742-54. doi: 10.1016/j.jpain.2012.05.011.
3
Membrane-initiated estradiol actions mediate structural plasticity and reproduction.膜介导的雌二醇作用介导结构可塑性和生殖。
Front Neuroendocrinol. 2012 Oct;33(4):331-41. doi: 10.1016/j.yfrne.2012.07.003. Epub 2012 Jul 22.
4
Keratinocyte expression of inflammatory mediators plays a crucial role in substance P-induced acute and chronic pain.角质细胞炎症介质的表达在 P 物质诱导的急性和慢性疼痛中起着关键作用。
J Neuroinflammation. 2012 Jul 23;9:181. doi: 10.1186/1742-2094-9-181.
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A potential role for integrin signaling in mechanoelectrical feedback.整合素信号在力电反馈中的潜在作用。
Prog Biophys Mol Biol. 2012 Oct-Nov;110(2-3):196-203. doi: 10.1016/j.pbiomolbio.2012.07.002. Epub 2012 Jul 20.
6
Transient decrease in nociceptor GRK2 expression produces long-term enhancement in inflammatory pain.伤害感受器 GRK2 表达的短暂下降可产生炎症性疼痛的长期增强。
Neuroscience. 2012 Oct 11;222:392-403. doi: 10.1016/j.neuroscience.2012.07.004. Epub 2012 Jul 13.
7
Activation of NMDA receptors leads to phosphorylation of TRPV1 S800 by protein kinase C and A-Kinase anchoring protein 150 in rat trigeminal ganglia.NMDA 受体的激活导致蛋白激酶 C 和 A-激酶锚定蛋白 150 使大鼠三叉神经节 TRPV1 S800 磷酸化。
Biochem Biophys Res Commun. 2012 Jul 27;424(2):358-63. doi: 10.1016/j.bbrc.2012.07.008. Epub 2012 Jul 10.
8
Tanezumab reduces osteoarthritic knee pain: results of a randomized, double-blind, placebo-controlled phase III trial.替扎尼布可减轻骨关节炎膝关节疼痛:一项随机、双盲、安慰剂对照 III 期临床试验结果。
J Pain. 2012 Aug;13(8):790-8. doi: 10.1016/j.jpain.2012.05.006. Epub 2012 Jul 10.
9
Estrogen in the anterior cingulate cortex contributes to pain-related aversion.前扣带皮层中的雌激素有助于与疼痛相关的厌恶。
Cereb Cortex. 2013 Sep;23(9):2190-203. doi: 10.1093/cercor/bhs201. Epub 2012 Jul 10.
10
Clinical improvement in a patient with neuromyelitis optica following therapy with the anti-IL-6 receptor monoclonal antibody tocilizumab.抗白细胞介素 6 受体单克隆抗体托珠单抗治疗视神经脊髓炎谱系疾病患者的临床改善。
Mod Rheumatol. 2013 Jul;23(4):827-31. doi: 10.1007/s10165-012-0715-9. Epub 2012 Jul 11.

疼痛的基本单位是细胞。

The fundamental unit of pain is the cell.

机构信息

Department of Medicine, Division of Neuroscience, University of California-San Francisco, San Francisco, CA, USA; Department of Oral and Maxillofacial Surgery, Division of Neuroscience, University of California-San Francisco, San Francisco, CA, USA.

出版信息

Pain. 2013 Dec;154 Suppl 1:S2-9. doi: 10.1016/j.pain.2013.05.037. Epub 2013 May 24.

DOI:10.1016/j.pain.2013.05.037
PMID:23711480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3858489/
Abstract

The molecular/genetic era has seen the discovery of a staggering number of molecules implicated in pain mechanisms [18,35,61,69,96,133,150,202,224]. This has stimulated pharmaceutical and biotechnology companies to invest billions of dollars to develop drugs that enhance or inhibit the function of many these molecules. Unfortunately this effort has provided a remarkably small return on this investment. Inevitably, transformative progress in this field will require a better understanding of the functional links among the ever-growing ranks of "pain molecules," as well as their links with an even larger number of molecules with which they interact. Importantly, all of these molecules exist side-by-side, within a functional unit, the cell, and its adjacent matrix of extracellular molecules. To paraphrase a recent editorial in Science magazine [223], although we live in the Golden age of Genetics, the fundamental unit of biology is still arguably the cell, and the cell is the critical structural and functional setting in which the function of pain-related molecules must be understood. This review summarizes our current understanding of the nociceptor as a cell-biological unit that responds to a variety of extracellular inputs with a complex and highly organized interaction of signaling molecules. We also discuss the insights that this approach is providing into peripheral mechanisms of chronic pain and sex dependence in pain.

摘要

分子/遗传时代见证了大量与疼痛机制相关的分子的惊人发现[18,35,61,69,96,133,150,202,224]。这刺激了制药和生物技术公司投资数十亿美元,开发增强或抑制许多这些分子功能的药物。不幸的是,这项努力的投资回报非常低。不可避免的是,该领域的变革性进展将需要更好地理解“疼痛分子”不断增加的数量之间的功能联系,以及它们与更多与之相互作用的分子之间的联系。重要的是,所有这些分子都存在于细胞及其相邻的细胞外分子基质中,它们是一个功能单元。用最近《科学》杂志上的一篇社论[223]的话说,尽管我们生活在遗传学的黄金时代,但生物学的基本单位仍可以说是细胞,细胞是理解与疼痛相关分子功能的关键结构和功能环境。这篇综述总结了我们目前对伤害感受器作为一个细胞生物学单元的理解,该单元通过信号分子的复杂和高度组织化相互作用对各种细胞外输入做出反应。我们还讨论了这种方法为慢性疼痛的外周机制和疼痛的性别依赖性提供的见解。