Background: Even though chemotherapeutic regimens show considerable importance, it may cause progressive,
continuing and sometimes irreversible peripheral neuropathy. Chemotherapy induced peripheral neuropathy
(CIPN) is comprised of sensory abnormalities that are most distressing issues. The mechanism associated with
CIPN pathogenesis is not completely revealed and its treatment is still questionable. The purpose of this review was
to investigate the role of mitochondria in CIPN.
Methods: This review is literature based that describes the mitochondrial mechanism underlying CIPN and the neuropathic
complications associated with different antineoplastic agents.
Results: For severe pain, a modification towards less efficient chemotherapeutic drugs could possibly be needed
and/or patients perhaps prefer to withdrawal therapeutic regimen. The epidemiology of CIPN is still debatable. The
major recurrent molecules causing CIPN are platinum based drugs including cisplatin and oxaliplatin, thalidomide,
bortezomib, vinka alkaloids and taxanes. Neuropathic pain is one of the symptoms of CIPN. Various neuropathic
disorders as well as CIPN are due to mitochondrial impairment, relevant impairment of Ca2+ signalling pathways
and reactive oxygen species (ROS) that ultimately leads to apoptosis.
Conclusion: The pathophysiology of CIPN is complicated as chemotherapeutic medications often involve combination
of drugs. With these combinatorial therapies cancer survivors develop continuing effects of CIPN which require
rehabilitation strategies for the recovery of patient’s condition and quality of life.