ASIC3 Protein May Be Involved in Development of Fibromyalgia Muscle Pain, Mouse Study Suggests

ASIC3 Protein May Be Involved in Development of Fibromyalgia Muscle Pain, Mouse Study Suggests
A mouse model of fibromyalgia, induced by temperature change and lacking the protein ASIC3, did not develop muscle pain, a study reports. The study suggests ASIC3-dependent changes in the molecules present in blood and urine could be useful biomarkers for the chronic pain disorder. Titled "ASIC3-dependent metabolomics profiling of serum and urine in a mouse model of fibromyalgia," the study was published in Scientific Reports. Because the underlying cause of fibromyalgia remains unknown, there currently are no biological markers that can provide information about the disease. That is a hindrance both for research and treatment of patients. Animal models may provide some clues, though. Previous studies that relied on acidic injections to induce pain had demonstrated that the protein ASIC3, or acid-sensing ion channel 3, plays a role in fibromyalgia-like pain. However, the protein's function in other models of fibromyalgia hasn't been investigated. The researchers behind the new report tested the effects of the ASIC3 protein in a mouse model of fibromyalgia induced by intermittent cold stress (ICS), in which rapidly changing temperatures lead to a sustained pain response. Wild-type mice developed fibromyalgia-like symptoms after ICS, including heightened sensitivity of their paws and muscles, as expected. Mice that had been engineered to lack the gene that codes for ASIC3 actually had similar responses with regard to their paws. But — crucially — they didn't display as severe muscle pain, which the researchers noted is the "core symptom" of fibromyalgia. The researchers then analyzed the small molecules in the mice's blood and urine, a strategy called metabolomics. Their goal was to find those that were affected by both ICS and ASIC3 — that is,
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