Chronic pain in rheumatoid arthritis (RA) is a multifaceted and persistent issue, significantly impacting patients' quality of life. Even when the inflammation associated with RA is managed through modern therapies, many patients continue to experience pain that is not fully alleviated. This pain, which can affect both the joints and non-articular regions, is driven by complex mechanisms that go beyond simple inflammation. Our research focuses on unravelling these underlying processes to offer new insights into effective pain management. One of the key elements in this chronic pain pathway is the ASIC3 ion channel, which is primarily expressed in peripheral sensory neurons. These neurons are responsible for detecting harmful stimuli and transmitting pain signals to the spinal cord and brain. The ASIC3 channel is particularly sensitive to changes in tissue acidity, a common feature in inflamed or damaged tissues, making it a central player in the sensation of pain, especially in conditions like RA. Our project aims to understand how ASIC3 contributes to pain sensitization, a process where pain signals become amplified, leading to heightened sensitivity and discomfort even in the absence of further inflammatory damage. This phenomenon, known as peripheral sensitization, plays a critical role in the transition from acute to chronic pain, a hallmark of RA.

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