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Numerous studies have reported the important role of glial modulation in pain.
In the following sections, we discuss the early evidence for epigenetic modulation in pain, as well as the therapeutic potential of targeting relevant epigenetic mechanisms (summarized in Figure 2).
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Previous studies investigating endogenous pain modulation in chronic pain populations have shown a potential deficiency of pain inhibitory system [ 3, 6, 7, 10, 12, 26, 50, 55].
The paper by Klug et al. [ 5] focuses on the issue of dysfunctional pain modulation in somatoform pain disorder patients.
We finally suggest that infusion of miR23b and NOX4 antibody may provide attractive diagnostic and therapeutic resources for effective pain modulation in neuropathic pain.
The activation of signal transduction cascades and the transcriptional changes in the DRG and the resultant alterations in the transmission properties of sensory neurons following peripheral nerve injury might be involved in modulation of pain signaling in acute and chronic pain conditions [2], [3].
We believe that this approach should be investigated in future studies, but it must be taken into account that we have recent evidence that therapeutic exercise and manual therapy to the cervical region produce positive effects on pain modulation in trigeminal areas and improving pain-free MMO [30,105].
The data suggested that OXT in the PAG could influence the L-Ek, M-Ek and β-Ep rather than DynA1 13 to participate in pain modulation, i.e. OXT in the PAG participate in pain modulation by influencing the L-Ek, M-Ek and β-Ep rather than DynA1 13.
This region appears to be involved in pain modulation.
Oxytocin may play a role in pain modulation.
Our pervious study had shown that AVP plays an important role in pain modulation in caudate nucleus (CdN).
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