by Chronic pain, a condition that lasts for more than six months, can significantly impact a person’s quality of life. While scientists have not fully understood why acute pain progresses to become chronic pain, recent research may offer some insights and a potential solution. Researchers from the Center for Translational Immunology at the University Medical Center (UMC) Utrecht have identified a process that underpins the transition from acute to persistent inflammation and found that boosting a type of vitamin B3 in cells could mitigate this progression.
The team focused on mitochondria, which have previously been linked to chronic pain, to investigate how inflammation affects these cellular powerhouses. Their findings revealed that a change in mitochondrial and metabolic function in sensory neurons, specifically the Dorsal root ganglion neurons (DRGs), disrupts the inflammation pathway that resolves pain. This disruption, known as hyperalgesic priming, causes pain to persist even after the initial inflammatory trigger has disappeared. Individuals with inflammatory and mitochondrial diseases are particularly susceptible to this condition.
The researchers discovered that mice primed for mitochondrial disturbance had low levels of nicotinamide riboside, a form of vitamin B3, once the initial pain inflammatory response subsided. Nicotinamide riboside is crucial for maintaining proper mitochondrial function, as it is converted to a chemical called NAD+.
By inhibiting mitochondrial respiration, reducing the expression of the ATPSCKMT gene, or supplementing NAD+ metabolites with increased nicotinamide riboside, the researchers were able to bypass chronic pain in mice. They observed that a cohort of mice that received nicotinamide riboside injections showed a slower response to pain stimuli, indicating that their hypersensitivity, a hallmark of chronic pain, had been regulated.
These findings pave the way for potential treatments that could prevent the development of chronic pain or reverse it. The researchers believe that further studies in this area could lead to therapeutic strategies that restore failing pain resolution pathways, effectively treating chronic inflammatory pain.
“In our study, we provide evidence that peripheral inflammation induces persistent mitochondrial and metabolic changes in sensory neurons, which affect the ability of neurons to resolve hyperalgesia induced by a subsequent inflammatory trigger,” explained the researchers. “Importantly, targeting mitochondrial respiration, scavenging reactive oxygen species, or supplementing with nicotinamide riboside (vitamin B3) both represent potential therapeutic strategies to restore failing pain resolution pathways, thereby treating chronic inflammatory pain.”
These promising findings could potentially revolutionize the way chronic pain is managed and provide much-needed relief for individuals suffering from this debilitating condition.
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1. Source: Coherent Market Insights, Public sources, Desk research
2. We have leveraged AI tools to mine information and compile it
Money Singh is a seasoned content writer with over four years of experience in the market research sector. Her expertise spans various industries, including food and beverages, biotechnology, chemicals and materials, defense and aerospace, consumer goods, etc.
