Qing-Jun is currently an Arthritis Research UK (ARUK) Senior Research Fellow in the Faculty of Biology, Medicine and Health, the University of Manchester. He is also the Academic Lead of the Biosciences International Summer School, BIO-SISS.
Qing-Jun obtained his first degree in Medicine (1996), MSc (1999) and M.D & Ph.D in Aviation Medicine and Aerospace Physiology (2002) in China. In 2003, Qing-Jun began his post-doctoral training (at the University of Manchester) to investigate the molecular mechanisms and pharmacological resetting of the biological clocks. In 2009, Qing-Jun was awarded a MRC Career Development Award Fellowship and started his own research group, focusing on circadian clocks, ageing and age-associated diseases. In 2015, Qing-Jun was awarded the Arthritis Research UK Senior Research Fellowship to continue his work into the roles of the cartilage circadian clocks in health and disease of the joint tissue.
Body clocks are the internal timing mechanism that drives endogenous circadian (near 24 hour) rhythms in sleep/wake cycle, hormone release and behaviour. During ageing, our body clocks gradually lose precision. Consequently, this loss of synchrony with the 24 hour light/dark environment imposes significant risks of developing human diseases, such as metabolic syndrome, obesity, diabetes, cardiovascular diseases and cancer. Research in this laboratory aims to 1) Identify mechanisms underlying age-related changes in circadian rhythms in both brain and peripheral organs. 2) Establish functional significance of various tissue clocks in coordinating local physiology. 3) Explore the hypothesis of targeting body clocks in order to ameliorate disease development or progression.
Age is the single biggest risk factor for a wide spectrum of diseases. The rapid population ageing needs better understanding of the various biological processes underlying age-related pathologies. Among these are circadian rhythms, the endogenous 24 hour cycles governing nearly all aspects of physiology and behaviour. In mammals (including humans), this rhythm is generated by the master clock (suprachiasmatic nucleus, SCN) in the brain, which entrains to the light/dark environment and co-ordinates the peripheral clocks in most major body organs and cells. Circadian clocks control ~10% of our transcriptome in a tissue-specific manner and disrupted circadian rhythms correlate with various pathologies. Mutations in core clock genes lead to metabolic syndrome, obesity, diabetes, premature ageing, and increased tumorigenesis.
My previous research focused on the molecular mechanisms of clock period regulation (Meng et al, 2008, Neuron) as well as the pharmacological resetting potentials of the circadian clock using compounds targeting various pathways (Meng et al 2008, J Cell Sci; Walton et al 2009, J Pharmacol Exp Ther; Meng et al 2010, PNAS; Li et al 2012, PLoS ONE). My current interest is the interface between ageing and circadian biology. In particular, I aim to address the molecular mechanisms underpinning the tissue-specific changes in circadian rhythms with advanced age. In the long term, outcomes from this work could aid therapeutic drug design against age-related ailments, such as osteoarthritis (Arthritis & Rheum 2013; Osteoarthritis & Carti 2015; J Clin Invest 2016; Nat Rev Rheum 2016), spinal disc degeneration (Annals Rheum Dis 2016), pulmonary fibrosis (Genes & Dev 2014), tendinopathies (Sci Rep 2014) and breast cancer.
Biosciences International Summer School, BIO-SISS
Final Year Course: Clocks, Sleep and Rhythms of Life
1st Year Zoology Tutorial
1st/2nd Year Neuroscience Tutorial
2nd Year Dissertation Students
Final Year Project Students
Erasmus Exchange Students