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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].