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Table 2 Key concepts and their relations to CRPS and NFκB

From: Applied information retrieval and multidisciplinary research: new mechanistic hypotheses in Complex Regional Pain Syndrome

Key concept Relation to CRPS Relation to NFκB
Substance P Locally elevated upon electrical C-fiber stimulation [16, 98] Induces NFκB mediated release of IL-6 and TNFα [103]
Calcitonin Gene-related Protein Systemically and locally elevated [13, 16, 98] Suppresses NFκB activity in thymic cells [104]
Bradykinin Systemically elevated [13] Activates NFκB [46, 51]
Vasoactive Intestinal Protein Systemically elevated [13] Locally decreased [99] Inhibits NFκB mediated chemokine production by macrophages [52]. Prevents NFκB binding to promoter site for NO [52]
Neuropeptide Y Systemically elevated [13] NPY-Y1-R expression is regulated by NFκB [54]
Neutral Endopeptidase Speculated to be decreased [19] No relation with NFκB described
Angiotensin Converting Enzyme Speculated to be decreased [19] Polymorphism in CRPS patients [79] Reduces NFκB activity [55]
TNFα Locally increased [10] Induced by NFκB [48], Activates NFκB [100]
IL-1β Locally increased [10] Stimulates NFκB mediated apoptosis in sympathetic neurons [101]
IL-6 Locally increased [10] Induced by NFκB [49]
Tryptase Locally increased [10] Induced by NFκB [103]
Free radicals Signs of free radical damage [24] Second messenger in NFκB activity [50, 59]
Nitric oxide Elevated after monocyte stimulation [102] NO reduces NFκB activity, but ONOO induces NFκB [45, 56, 57]
Protons (acidosis) Lactate increased in skin [20] Influences NFκB activity [22, 61, 62]
α -receptor Up-regulated in analgesic skin ([72] Pro-inflammatory responses mediated through NFκB [68-70]
Sympathetic neuron Speculated to be damaged in CRPS [105] NFκB mediates Il-1βinduced apoptosis [101]
NMDA receptor Role in development of central sensitization [28]. NFκB is involved in the up-regulation of some types of NMDA receptors [63].