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Jun-Ming Zhang is Professor, Vice Chair for Research in Anesthesia, and Endowed Chair of Anesthesia Research and Education in the Department of Anesthesiology at the University of Cincinnati College of Medicine. He obtained his Medical Degree from Shandong University, a Master’s Degree in Neurophysiology from Peking Union Medical College and the Chinese Academy of Medical Sciences, and completed a postdoctoral fellowship in Neurophysiology of Pain at Yale University School of Medicine, where he began basic pain research. At the University of Cincinnati, he serves as Principal Investigator in the Pain Research Center, leading studies on the physiology and pathophysiology of neuropathic pain, sympathetic regulation of inflammatory responses in pain, mechanisms and management of low back pain, sodium channels, ectopic discharges, and pathological pain.
Zhang’s laboratory employs rat and mouse models to investigate activity-dependent sympathetic sprouting, the neural and chemical basis of pathologic pain in conditions such as complex regional pain syndrome, the roles of inflammation and Nav1.6 sodium channels in chronic pain, and neural-immune interactions. His recent work includes translational human research on peripheral pain mechanisms, including the sympathetic system, immune responses, and spontaneous activity in sensory neurons. He has secured major NIH funding, including a five-year $3.1 million grant and the Javits Neuroscience Award. Key publications include the highly cited “Cytokines, inflammation, and pain” (2007, International Anesthesiology Clinics), “Mechanical and thermal hyperalgesia and ectopic neuronal discharge after chronic compression of dorsal root ganglia” (1999, Journal of Neurophysiology), “Neuropathic pain: early spontaneous afferent activity is the trigger” (2005, Pain), and recent papers such as “Vascular motion in the dorsal root ganglion sensed by Piezo2 sensed by vascular motion” (2025, Neuron), “Mineralocorticoid Receptor Antagonism Reduces Inflammatory Pain Measures in Mice” (2024, Neuroscience), and “The Antinociceptive Effect of Sympathetic Block is Mediated by Transforming Growth Factor beta” (2023, Neuroscience Bulletin). His research has significantly advanced understanding of pain mechanisms, contributing to potential new treatments for neuropathic and inflammatory pain conditions.

Photo by Osarugue Igbinoba on Unsplash
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