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Personal profile

General

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.

Employment

  • 2017-present, lecturer, Aston university
  • 2014-2016, Lecturer, University of Aberdeen
  • 2009-2013, MRC independent research fellow, University of Cambridge
  • 2002-2008, Postdoctoral research fellow, University of Cambridge

Teaching Activity

  • System neuropharmacology NE2002
  • Key skills in neuroscience NE1003
  • Neuropharmacology PH3601
  • Introduction to physiology and pharmacology MS1000
  • Molecular basis of pain NE3005

Qualifications

FHEA, Aston University, 2018

Ph.D, Tongji Medical College, Huazhong University of Science and Technology 2001

Membership of Professional Bodies

British Neuroscience Association

The Physiological Society

Funding Applications and Awards

Versus Arthritis

Royal society 

Medical research council

Research Interests

I am interested in the molecular mechanisms of pain and itch. Pain is one of the most common medical conditions affecting 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 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 targets for analgesics.

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 aspect of my research is to decipher the molecular links between the pain signalling system and the metabolic system. Pain sensitivity is influenced by the body metabolic status. Indeed, pain is often reported in old people known to have a lower metabolic rate. Metabolic disorders such as diabetic neuropathy are often associated with enhanced pain sensitivity. Reciprocally, pain signalling modulates body metabolism and promotes diet-induced obesity. Understanding how pain sensitivity is determined by the metabolic status offers a unique means to unravel the mechanisms of pain and to identify novel therapeutic targets.

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.

Contact Details

Telephone: +44 (0) 121 204 4828
Email:  x.zhang39@aston.ac.uk
Room: MB354

Office Hours: Normal working hours

Keywords

  • RM Therapeutics. Pharmacology
  • QP Physiology

Fingerprint Dive into the research topics where Xuming Zhang is active. These topic labels come from the works of this person. Together they form a unique fingerprint.

Ion Channels Medicine & Life Sciences
Hot Temperature Medicine & Life Sciences
Sensory Receptor Cells Medicine & Life Sciences
Pain Medicine & Life Sciences
Bradykinin Medicine & Life Sciences
Hyperalgesia Medicine & Life Sciences
Chemical activation Chemical Compounds
Transient Receptor Potential Channels Medicine & Life Sciences

Network Recent external collaboration on country level. Dive into details by clicking on the dots.

Research Output 2005 2019

Direct Gα q Gating Is the Sole Mechanism for TRPM8 Inhibition Caused by Bradykinin Receptor Activation

Zhang, X., 18 Jun 2019, In : Cell Reports. 27, 12, p. 3672-3683.e4

Research output: Contribution to journalArticle

Open Access
File
Bradykinin Receptors
Bradykinin
Chemical activation
Programmable logic controllers
Crosstalk

Ca2+ regulation of TRP ion channels

Hasan, R. & Zhang, X., 23 Apr 2018, In : International Journal of Molecular Sciences. 19, 4, 1256.

Research output: Contribution to journalReview article

Open Access
File
Transient Receptor Potential Channels
Ion Channels
Ions
G-Protein-Coupled Receptors
Physiological Phenomena

Calmodulin is responsible for Ca2+-dependent regulation of TRPA1 channels

Hasan, R., Leeson-Payne, A. T. S., Jaggar, J. H. & Zhang, X., 23 Mar 2017, In : Scientific Reports. 7, 12 p., 45098.

Research output: Contribution to journalArticle

Open Access
File
Calmodulin
Sensation Disorders
Ion Channels
Pain

Potential role of CXCL10/CXCR3 signaling in the development of morphine tolerance in periaqueductal gray

Wang, W., Peng, Y., Yang, H., Bu, H., Guo, G., Liu, D., Shu, B., Tian, X., Luo, A., Zhang, X. & Gao, F., 1 Oct 2017, In : Neuropeptides. 65, p. 120-127

Research output: Contribution to journalArticle

Open Access
File
Periaqueductal Gray
Microglia
Morphine
Neurons
Minocycline

Spinal CX3CL1/CX3CR1 may not directly participate in the development of morphine tolerance in rats

Peng, Y., Guo, G., Shu, B., Liu, D., Su, P., Zhang, X. & Gao, F., 1 Nov 2017, In : Neurochemical Research. 42, 11, p. 3254–3267

Research output: Contribution to journalArticle

Open Access
File
Morphine
Rats
CX3C Chemokines
Spinal Cord
Chemokine CX3CL1