Chronic pain is a debilitating condition and represents a clinical challenge for the practicing physician. The long-term goal of my research is to understand the mechanisms underlying the development of chronic pain. Increasing evidence has demonstrated that calcium signal contributes to the induction and maintenance of pain hypersensitivity. My research has been concentrated on the role of store-operated calcium channels (SOCs), calcium-selective cation channels that comprise three pore-forming subunits Orai1/2/3 and two calcium sensors STIM1 and STIM2, in pain plasticity. Currently, we are identifying endogenous upstream molecules of SOC signaling and exploring functional consequences of SOC channel activation. These studies will extend our knowledge of how SOC signaling modulates pain and will provide novel insights into mechanisms underlying chronic pain. We hope to identify SOC channels as drug targets and develop new approaches to therapeutic intervention for chronic pain associated with nerve injury and diseases.
- Title
- Associate Professor
- Area of Study/Expertise
- Chronic Pain
- hh480@njms.rutgers.edu