After my first degree of MB ChB (Wuhan University School of Medicine), I left China to pursue scientific training in various labs in South Africa, and then UK. My research activity and publications led to the award of PhD degree at Faculty of Life Sciences, the University of Manchester, soon after I was awarded a prestige 5-year RCUK fellowship, which enabled me to establish independent research in Gene Regulation and Sigalling in Cardiovascular Diseases. At the end of the 5 year Fellowship I took a position as Lecturer,  Senior Lecturer, and then promoted to Chair as Professor of Molecular Cardiology. I am the Deputy Head of  Cardiovascular Sciences Division at Faculty of Biology, Medicine and Health, the University of Manchester, and I am also an editor of British Journal of Pharmacology.  

From Signal transduction to gene regulation in the diseased heart

Despite major progress in medical science, cardiovascular disease (CVD) remains the biggest cause of death worldwide, with heart failure (HF) in particular representing its fastest growing subclass with the highest morbidity and mortality over the past decade. Heart failure (HF) affects 2–3% of the population in industrialized countries with a marked rise in those aged 65. It has been estimated that 15 million people in the EU suffer from HF, which leads to a significant financial burden of approximately 30 billion Euro/year on the EU health services. Its incidence is still rising rapidly due to increases in three major risk factors: population ageing, obesity and diabetes. HF has a dismal prognosis, with patients dying from progressive pump failure or ventricular arrhythmias. Unfortunately, the current medications for treating HF do not increase survival, regardless of the treatment, 50% of individuals die within 5 years of developing HF. In an era where morbidity and mortality from other CVD conditions are decreasing, deaths from HF are increasing. There is therefore an urgent need to develop new and more effective strategies and targets for prevention and treatment of this condition.

To meet this pressing need, my group focuses on gaining a better understanding of pathological mechanisms underlying HF. Our main research areas lie in three disease states, which are prerequisites for the development of HF: 1) cardiac hypertrophy and associated ventricular arrhythmias; 2) cardiac ischemia/reperfusion injury; 3) diabetes and/or obesity associated cardiomyopathy. We aim to elucidate pathophysiological role of the individual component of signalling cascades and subsequent gene regulation profiles in these disease states, and reveal molecular basis for protecting or destructing cardiomyocytes in heart diseases. Our approaches include genome-editing animal models, primary cardiomyocytes differentiated from human iPSCs, larger genomic screening (ChIP-seq, RNA sequencing) and computer simulations. Our study will provide a solid ground for the development of effective pharmacological or gene-based therapies, ultimately improving clinical treatments for those patients with cardiac diseases.

Omic technologies and resources BIOL21152

Pharmacology Practical Unit BIOL31661

Academic Tutorials Year 2 B20000

PBL Medical School Year 1