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]. |