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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 obtaining Ph.D and M.D degrees.

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

  • Receptors and ion channels NE2011
  • Molecular basisi of pain NE3005
  • Key skills in neuroscience NE1008
  • Neuropharmacology PH3601
  • Introduction to physiology and pharmacology MS1000

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

BBSRC

MRC

Versus Arthritis

Royal society 

 

Research Interests

I am interested in the molecular and cellular 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 appealing 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 acute and chronic pain such as disabling chronic arthrits pain. This research has led to several high impact publications, such as Neuron, Nature Cell Biology, EMBO J and Journal of Neuroscience. Our findings have promoted our understanding of molecular underpinnings of pain with therapeutic implications.

Secondly, we are interested in the regulation of neuronal excitability. Firing of neurons is fundamental to many physiological functions in the nervous system. Abnormal neuronal firing underpins many conditions in the nervous system such as inflamamtory pain and neuropathic pain. Neuronal firing is collectively determined by a cohort of voltage-gated Na+, K+ and Ca2+ channels. The activities of these ion channels are subjected to both rapid posttranslational modifications and long-term gene dysregulation triggered by a variety of neuronal signalings. We aim to reveal the molecules and signaling events crucial to aberrant neuronal firing in chronic pain.

The third 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 fourth 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: MB434N

 

Keywords

  • RM Therapeutics. Pharmacology
  • QP Physiology

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