Understanding the role of mitochondria in the pathogenesis of chronic pain

Abstract

Chronic pain is a major public health problem. Mitochondria play important roles in a myriad of cellular processes and mitochondrial dysfunction has been implicated in multiple neurological disorders. This review aims to provide an insight into advances in understanding of the role of mitochondrial dysfunction in the pathogenesis of chronic pain. The results show that the five major mitochondrial functions (the mitochondrial energy generating system, reactive oxygen species generation, mitochondrial permeability transition pore, apoptotic pathways and intracellular calcium mobilisation) may play critical roles in neuropathic and inflammatory pain. Therefore, protecting mitochondrial function would be a promising strategy to alleviate or prevent chronic pain states. Related chronic inflammatory and neuropathic pain models, as well as the spectral characteristics of current fluorescent probes to detect mitochondria in pain studies, are also discussed.

8-O-Acetyl Shanzhiside Methylester From Lamiophlomis Rotata Reduces Neuropathic Pain by Inhibiting the ERK/TNF-α Pathway in Spinal Astrocytes

“…What is worth noting is the improvement of mitochondrial energy metabolism (Jiang et al, 2010 , 2011 ; Kang et al, 2012 ). Mitochondrial dysfunction is also implicated in the pathogenesis of NP, and protecting mitochondrial function is a promising strategy to alleviate or prevent chronic pain (Sui et al, 2013 ). In light of this, we proposed that the regulation of mitochondrial disorder and neuron apoptosis might be another mechanism for 8-OaS analgesia, which remains to be explored in future studies.…”

Ocular neuropathic pain

“…The diversity of systemic diseases associated with centralised corneal pain suggests that they may share underlying pathogenetic vulnerabilities. Reports of mitochondrial dysfunction in patients with SS 95 and fibromyalgia 96 and in those with chronic neuropathic pain 97 suggest a possible link, whether one of association or causation.…”

Histamine H4 receptor agonist‐induced relief from painful peripheral neuropathy is mediated by inhibition of spinal neuroinflammation and oxidative stress

“…MnSOD and CuZnSOD rapidly scavenge and dismutate superoxide, acting as a first line of defence against electron transport chain‐derived oxidative stress (Zelko et al ., ; Candas and Li, ). MnSOD is localized within the mitochondrial matrix, a site of significant oxygen‐free radical production during energy metabolism and also supposed to be linked to the aetiology of neuropathic pain (Sui et al ., ). CuZnSOD is located in the cytosol, in greater concentration than MnSOD, and functions to detoxify superoxide anion generated from many sources.…”

“…The different changes in the contents of MnSOD and CuZnSOD following nerve injury may reflect their respective subcellular localization and site of action. In contrast to the cytosolic localization of the CuZnSOD isoform, MnSOD has a mitochondrial localization (Zelko et al, ), and mitochondrial dysfunction has been linked to the aetiology of neuropathic pain (Sui et al, ). The SOD enzyme working at mitochondrial levels, even if less abundantly expressed, appears the most likely to play a prominent protective role on SNI mice.…”