Involvement of TRP channels on fibromyalgiainduced pain

Abstract

Fibromyalgia (FM) is a common chronic pain  syndrome affecting up to 2% of the adult population. Several factors such as excessive oxidative stress and  overload calcium ion (Ca2+) influx play main roles in  the etiology of FM. Several pharmaceutical drugs such  as antidepressants and voltage-gated calcium channel  blockers are recommended for the treatment of FM;  however, they fail to produce a satisfactory response in  patients with FM because of the unclear etiology of the  disease. Transient receptor potential (TRP) channels  have six subfamilies and 27 members in human. Most of  these channels are responsible in dorsal root ganglia  (DRG) neurons for the Ca2+ permeation especially in  neuronal cells. Expression level of the TRPM2 and  TRPV1 channels are high in the DRG neurons and they  show oxidative stress dependent activation (Tan and  McNaughton 2016; Santos et al. 2018). The TRPM2  and TRPV1 channel expression levels in the DRG  increased in different types of pain. Selenium as an  antioxidant trace element is implicated as a  neuroprotective agent in peripheral pain through the  inhibition of apoptosis and regulation of the TRPM2  and TRPV1 channels (Kahya et al. 2017). Since a  decade, a recent theory have argued that both supporting  of intracellular antioxidant system and extracellular  antioxidant administration may helpful in fibromyalgia  for the inhibition of TRP channels mediated Ca2+ influx  (Yuksel et al. 2017). In the oral presentation, I discussed  novel effects of selenium on the treatment of irregular  oxidative status and fibromyalgia by the regulation of  TRPM2 and TRPV1 channels in rats.  In conclusion, present literature information  indicated that protective effects of selenium on TRPM2  and TRPV1 channels may novel approach to treat FM induced  pain and mitochondrial oxidative stress.  However, the subject should be clarified by further  studies.