A new study led by researchers at McGill University in Canada recently revealed that peripheral neuropathy (nerve damage) is associated with a mitochondrial dysfunction and a bioenergetic impairment. The study was published in the journal Molecular Pain and is entitled “Mitochondrial and bioenergetic dysfunction in trauma-induced painful peripheral neuropathy.”
Medical disorders characterized by painful peripheral neuropathy (damage to a nerve outside the brain and spinal cord) have been associated with mitochondrial dysfunction, including diabetic neuropathy, chemotherapy induced neuropathy, and HIV-associated sensory neuropathy. Mitochondria are small cellular organelles in the body responsible for the production of energy through the process of respiration. Mitochondria dysfunction can impair the cellular energy metabolism, affecting several organs and cells, like neurons, potentially leading to cell death and neurodegeneration. The lack of energy can cause a reduction in the activity of sodium-potassium pumps that ultimately lead to a condition that triggers the spontaneous activity of sensory neurons resulting in neuropathic pain.
The goal of the study was to determine whether mitochondrial dysfunction is linked to pain in trauma-induced peripheral neuropathy. The research team conducted a time-course analyzing mitochondrial function and bioenergetics in a mouse model of trauma-induced neuropathic pain – the partial sciatic nerve ligation model.
Researchers found that traumatic nerve injury causes an increase in the metabolic needs of the nerve that lead to increased glycolysis (oxidation of glucose, sugar) and oxygen consumption; these, in turn lead to conditions of acidosis (increased acidity in body fluids) and hypoxia (deficit of oxygen). This increased metabolic need of the damaged nerve is in line with a bioenergetic dysfunction, characterized by a reduced glycolytic capacity and little ability to respond to an increase in energy demand, and a mitochondrial dysfunction, characterized by a decline in energy production.
In conclusion, researchers report that traumatic peripheral nerve injury leads to a mitochondrial and bioenergetic dysfunction. The team suggests that therapeutic agents able to normalize these two dysfunctions might have a clinical benefit in patients experiencing pain due to injured nerves. The authors also add that within the group of potential therapeutic agents, drugs that act preferentially on acidic tissues (such as those developed for cardiac arrhythmia) might be more adequate for the treatment of injured nerves without having an impact on healthy tissues.
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