Professor Khalid Naseem
- Position: Professor
- Areas of expertise: Blood platelets, thrombosis, cell signalling, lipoproteins; flow cytometry, intravital microscopy.
- Email: K.Naseem@leeds.ac.uk
- Location: 7.03a LIGHT
Khalid performed his undergraduate studies in Applied Biotechnology at Thames Polytechnic. He then studied for a PhD, and performed his post-doctoral research training, at the Royal Free Hospital School of Medicine under the supervision of Professor Richard Bruckdorfer.
In 2000 he moved to the University of Bradford to take up his first independent post as a Lecturer in Biomedical Sciences, where he held a number of departmental and university-wide roles while developing an independent research programme. In 2007 he was awarded a personal Chair at the University of Bradford.
In 2009, Khalid was appointed as Foundation Chair in Biomedical Sciences at the Hull York Medical School (University of Hull). During his time at Hull he launched, and was the first director of, the Centre for Cardiovascular and Metabolic Research and was later appointed as Associate Dean for Research.
In 2017, Khalid moved to Leeds to take up the post of Professor of Cardiovascular Biology.
Blood platelets play a key role in the initiation and progression of atherosclerosis, the pathology that underpins a spectrum of cardiovascular diseases. Individuals with cardiovascular diseases succumb to changes in the blood and vessel wall that enhance platelet activation and promote thrombosis. The focus of research in Khalid's laboratory is identifying the molecular and cellular mechanism(s) that lead to platelet hyperactivity, which can in turn contribute to atherogenesis and atherothrombosis in the context of metabolic disorders such as dyslipidaemia and dysglycaemia.
Much of the work is focussed on the role of a surface protein called cluster of differentiation 36 (CD36). This multifunctional receptor acts as a fatty acid transporter, but also as a scavenger receptor that sensors immunological and metabolic changes in the blood. While the receptor binds a wide variety of factors including oxidised lipids, glycated proteins and malaria-infected red blood cells, it is unclear how these different ligands influence platelet function or how it impacts on disease process. We are currently working on dissecting the mechanisms by which these diverse ligands alter platelet function through CD36 binding.
Aligned to understanding the role of CD36 we are also examining whether changes in the blood environment leads to immunometabolic reprogramming of platelets. Platelets demonstrate metabolic plasticity that allow them to efficiently utilise available metabolic fuels, variations in fuel availability can modify cell function. Through collaborations with clinical scientists studying metabolic disorders such as diabetes and coronary heart disease we are examining if platelets undergo immunometabolic reprogramming and how this impacts on disease progression.
Critical to our research is the need to improve the understanding and treatment of atherothrombotic disease. A better understanding of the mechanisms that drive platelet hyperactivity in the context of disease will aid in the development or more targeted strategies for controlling thrombosis.
Our work is supported through research grants from the British Heart Foundation and Heart Research UK.
- BSc (Hons)
- Platelet Society
- British Society for Haemostasis and Thrombosis
- International Society for Thrombosis and Haemostasis
- British Atherosclerosis Society
Khalid chairs the techahing group for the Discovery and Translational Science Department within the Institute for Cardiovascular and Metabolic Research. He also contributes to various PhD training programmes.
Research groups and institutes
- Leeds Institute of Cardiovascular and Metabolic Medicine
- Discovery and Translational Science
- British Heart Foundation - Cardiovascular research
<li><a href="//phd.leeds.ac.uk/project/194-the-role-of-platelet-dysfunction-in-promoting-diabetic-thrombo-inflammation.">The role of platelet dysfunction in promoting diabetic thrombo-inflammation.</a></li>