Bsc; MRes; PhD
Senior postdoctoral researcher
My research interest is to understand inflammatory responses in inherited heart muscle diseases including hypertrophic and dilated cardiomyopathy (ie HCM and DCM). Among these, HCM is the most common disorder in the clinic.
The symptoms that many HCM patients experience include shortness of breath, chest pain, and fatigue, which are not always controlled by current therapies. In addition, there is a small risk of developing a life-threatening abnormal heart rhythm and sudden cardiac death. The clinic hallmarks include accumulative tissue scarring and heart muscle enlargement. A faulty gene, which is often identified in heart muscle cells, is believed to be causative. However, patients who share the mutation differ considerably in the types and severity of their symptoms. Immune cell populations and their ability to regulate inflammatory responses in the heart could be heterogeneous, which may provide an explanation for this discrepancy. My current research aims are:
- To investigate whether immune cells play a role in hypertrophy, myocardial fibrosis and cardiac dysfunctions in HCM;
- To identify immune cell-specific targets for developing immunotherapies for HCM;
My approaches to achieve these goals are:
- To employ various animal models to study the role of individual immune cell populations in HCM;
- To take advantage of our state-of-the-art facilities to trace physiological and pathological changes in animal models of HCM;
- To develop a series of in vivo, ex vivo, and in vitro imaging tools for better characterising cardiac immune cells and inflammatory responses in situ;
- To establish a profile of genomic, proteomic, and metabolic data of cardiac immune cell populations in healthy and diseased hearts;
- To prove the concept of cardiac immunotherapy using animal models and pharmacological reagents targeting immune cells;
I have been working as a postdoctoral researcher in the group of Prof Houman Ashrafian and Prof Hugh Watkins since 2014, focusing on deciphering chronic inflammatory responses in HCM. I also act as the chairman of the Oxford Chinese Life Science Society (OCLSS) and organise activities for Chinese students and scholars in life science. I was previously a postdoctoral researcher at the MRC Human Immunology Unit at the MRC Weatherall Institute of Molecular Medicine (WIMM) with a specific focus on lymphatic endothelial functions during inflammation. Prior to this, I completed my first postdoctoral training at the University of Birmingham and obtained my PhD in Newcastle University in the field of cardiovascular diseases and inflammation.
TNF-derived peptides inhibit tumour growth and metastasis through cytolytic effects on tumour lymphatics.
Lu W. et al, (2019), Clin Exp Immunol, 198, 198 - 211
Syk and Src family kinases regulate C-type lectin receptor 2 (CLEC-2)-mediated clustering of podoplanin and platelet adhesion to lymphatic endothelial cells.
Pollitt AY. et al, (2014), J Biol Chem, 289, 35695 - 35710
Megakaryocyte-specific deletion of the protein-tyrosine phosphatases Shp1 and Shp2 causes abnormal megakaryocyte development, platelet production, and function.
Mazharian A. et al, (2013), Blood, 121, 4205 - 4220
Dominant role of the protein-tyrosine phosphatase CD148 in regulating platelet activation relative to protein-tyrosine phosphatase-1B.
Mori J. et al, (2012), Arterioscler Thromb Vasc Biol, 32, 2956 - 2965
Mice lacking the ITIM-containing receptor G6b-B exhibit macrothrombocytopenia and aberrant platelet function.
Mazharian A. et al, (2012), Sci Signal, 5