School of Life & Health Sciences Aston University BirminghamB4 7ETUK
Tel: 0121 204 4828 Email:email@example.com Room: MB354
Office Hours: Normal Working Hours
I joined Aston university as a lecturer in neuroscience in 2017. Prior to that, I was a lecturer at the University of Aberdeen after a period of independent research funded by an MRC new investigator award at the University of Cambridge. I carried out my postdoctoral research with Prof. Peter McNaughton at the University of Cambridge after received a Ph.D degree in China.
Associate fellow in Higher Education, University of Aberdeen, 2016
Ph.D Tongji Medical College, Huazhong University of Science and Technology, China, 2001
2002-2008, Postdoctoral research fellow, University of Cambridge
I am interested in the molecular mechanisms of pain and itch. Pain is one of the most common medical conditions affecting the quality of life of many patients. Pain signals are generated by specialized sensory receptors (or nociceptors) on peripheral sensory nerve endings followed by transmission via afferent nerve fibres to the brain in the central nervous system where pain is interpreted. Damage to and interference with the pain pathway can markedly affect pain sensation, leading to either enhanced pain (hyperalgesia) or pain inhibition (analgesia). Notably, a family of Transient Receptor Potential (TRP) ion channels (e.g. TRPV1, TRPA1) have emerged as critical sensory nociceptors responsible for detecting noxious thermal, chemical and mechanical stimuli. TRP ion channels have thus become analgesic drug targets. The first line of my research is to investigate the function and modulation of TRP ion channels in sensory neurons under physiological and disease conditions, and how they contribute to hyperalgesia. This research has led to several high impact publications, such as Neuron, Nature Cell Biology, EMBO J and Journal of Neuroscience. They have promoted our understanding of molecular underpinnings of pain with therapeutic implications.
The second line of my research is to understand metabolic modulation of the pain pathway. The transmission of electrical pain signals and constant recharging of neurons require a great deal of metabolic energy. The pain pathway is thus readily influenced by body metabolic conditions. As an example, pain is often reported in old people known to have lower metabolic rate. Metabolic disorders such as obesity and diabetic neuropathy are often associated with enhanced pain sensitivity. We will aim to decipher the molecular links between pain and metabolism.
The third area of interest is to understand the mechanisms of itch (pruritus). Itch is another somatic sensation and is a common symptom associated with many diseases such as cholestatic liver disease and diabetes. Itch is closely linked to pain, but is transduced via distinct neural pathways. Interestingly, TRP ion channels, such as TRPV1 and TRPA1, not only mediate pain, but also carry itch. We are interested in the molecules and signalling pathways that mediate itch.
We use electrophysiology, molecular biology, protein biochemistry and imaging combined with behavioural approaches to address our queries.
Medical Research Council