Background: Peripheral neuropathies are a group of diseases characterized by
malfunctioning of peripheral nervous system. Neuropathic pain, one of the core manifestations of
peripheral neuropathy remains as the most severe disabling condition affecting the social and daily
routine life of patients suffering from peripheral neuropathy.
Method: The current review is aimed at unfolding the possible role of mitochondrial dysfunction in
peripheral nerve damage and to discuss on the probable therapeutic strategies against neuronal
mitotoxicity. The article also highlights the therapeutic significance of maintaining a healthy
mitochondrial environment in neuronal cells via pharmacological management in context of peripheral neuropathies.
Results: Aberrant cellular signaling coupled with changes in neurotransmission, peripheral and central sensitization are
found to be responsible for the pathogenesis of variant toxic neuropathies. Current research reports have indicated the
possible involvement of mitochondria mediated redox imbalance as one of the principal causes of neuropathy aetiologies.
In addition to imbalance in redox homeostasis, mitochondrial dysfunction is also responsible for alterations in
physiological bioenergetic metabolism, apoptosis and autophagy pathways.
Conclusions: In spite of various etiological factors, mitochondrial dysfunction has been found to be a major
pathomechanism underlying the neuronal dysfunction associated with peripheral neuropathies. Pharmacological
modulation of mitochondria either directly or indirectly is expected to yield therapeutic relief from various primary and
secondary mitochondrial diseases.