What is it about?
This research focuses on a protein called NaV1.7, found in nerve cells, which plays a crucial role in sending pain signals in conditions like nerve injury or chemotherapy-induced nerve damage. So far, attempts to block NaV1.7 directly with drugs haven't been successful. However, we've discovered a unique part of NaV1.7 (we call it the CRS domain) that interacts with another protein, CRMP2. When we blocked this interaction, we were able to turn down the pain signals. We also developed a small peptide (a piece of a protein) that mimics the CRS domain, and found that this reduced pain signals in both animal models and nerve cells from monkeys without affecting normal pain sensations or movement. Additionally, we packaged a gene that encodes for this CRS peptide into a virus, which we used to deliver the gene into nerve cells. This approach also reduced pain signals in our models. Overall, these findings suggest that targeting the CRS domain of NaV1.7 could be a new way to treat chronic nerve pain.
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Why is it important?
Our approach's applicability to real-world solutions for chronic pain is underscored by our gene therapy successfully reducing NaV1.7 function in macaque DRG neurons, which are identical in sequence to human NaV1.7.
Perspectives
Small molecules have failed to deliver against the rising burden of pain. With the advances in gene therapy and genome editing technologies, we are now well positioned to move the needle for chronic pain management using gene therapy for chronic pain.
Rajesh Khanna
New York University
Read the Original
This page is a summary of: Identification and targeting of a unique Na
V
1.7 domain driving chronic pain, Proceedings of the National Academy of Sciences, July 2023, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2217800120.
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