|1986-1991 B.S.at Tongji Medical University|
1991-1996 Resident physician at Department of Rheumatology, China-Japan Friendship Hospital
1996-1999 M.S. at Beijing Institute of Geriatrics of Ministry of Health
1999-2002 Attending physician at Department of Pulmonary Disease, Beijing Hospital
2002-2007 Ph.D. at School of Biological and Biomedical Science, University of Durham
2007-2008 Research Associate at Structural Genomics Consortium, University of Oxford
2008-2018 Research Associate at Department of Biochemistry, University of Cambridge
2018.9- Assistant Professor, PI at School of Life Science and Technology, ShanghaiTech University
|Chronic pain is a rising health problem that afflicts ~10% of the population. There are several different classes of chronic pain, including inflammatory pain following tissue injury, neuropathic pain following nerve, spinal cord and brain injury, cancer pain and pain induced by drug treatment. Chronic pain is typically characterized by hyperalgesia and allodynia, which results from altered neuronal activity. The development of neuroinflammation is responsible for generating and sustaining the sensitization of nociceptive neurons that leads to chronic pain. Neuroinflammation occurs in the peripheral and central nervous system, and is characterized by infiltration of leukocytes and increased production of inflammatory mediators at these sites. In the peripheral neuroinflammation, inflammatory mediators activate several kinases, which cause peripheral sensitization through the modulation of key transduction molecules such as transient receptor potential (TRP) cation channels TRPA1, TRPV1 and TRPM8, as well as key conduction molecules such as the voltage-gated sodium channels Nav1.7, Nav1.8 and Nav1.9. Currently, the treatment of intractable neuropathic pain still relies on classical analgesics, including morphine or antiepileptic drugs, which have limited efficacy and numerous side effects. Targeting the processes and molecules that are involved in neuroinflammation could lead to better treatments for chronic pain.|
Antibiotic resistance of pathogenic bacteria is a growing clinical problem, exacerbated by insufficient development of new antibiotics. Drug efflux pumps in the bacterial cell envelope play important roles in intrinsic or acquired drug resistance to a wide variety of currently available antimicrobial agents, which is one of the major causes of multidrug resistance. The lack of structural and mechanistic information has hindered the development of drugs to block these pumps.
Our group is interested in the elucidation of the structure and mechanism of chronic pain related ion channels, as well as tripartite multidrug efflux pumps of Gram-negative pathogenic bacteria, using cryo-electron microscopy and X-ray crystallography, as well as other biophysics and biochemistry methods. This information will guide structure-based drug design.
1. Du D, Wang-Kan X, Neuberger A, van Veen HW, Pos KM, Piddock LJV, Luisi BF. Multidrug efflux pumps: structure, function and regulation. Nat Rev Microbiol. 2018, 16(9):523-539.