![Aortic aneurysm and thrombosis.](https://www.mmu.ac.uk/sites/default/files/styles/page_header_half/public/2021-04/Thrombosis.jpg?h=f3f188b5&itok=ldK0hNrD)
Research: Thrombosis
Understanding the molecular mechanisms that underpin thrombosis, and aiming to identify new treatments of cardiovascular disease.
About
Cardiovascular disease (CVD) is the leading cause of morbidity worldwide and the most common cause of premature death. 80% of the deaths - around 15 million globally per year - are caused by the formation of a blood clot that blocks an artery leading to a heart attack or stroke.
The majority of these clots arise when atherosclerotic plaques within the artery wall rupture or erode exposing extracellular matrix proteins.
Circulating platelets bind to these proteins and become activated, leading to the recruitment of more platelets and the generation of a platelet-rich clot.
![Image of platelet activation](/sites/default/files/styles/1440px/public/2021-04/Understanding-molecular-mechanisms-underlying-platelet-activation--Dr-Sarah-Jones-and-Dr-Amanda-Unsworth-2.jpg?itok=FRtIjTbV)
Background
Platelets are the small anucleate cells, which normally circulate in the blood and play a central role in haemostasis, the process of preventing blood loss. At sites of vascular injury (when damage occurs to the blood vessel wall), they rapidly form blood clots to prevent excess bleeding and haemorrhage. Unwanted platelet activation however, for example following atherosclerotic plaque rupture or following endothelial dysfunction, results in thrombosis.
Thrombosis is the pathological formation of an unwanted blood clot that can block the blood vessel. Thrombosis can be classified according to the underlying cause, namely arterial thrombosis, which is mediated by plaque rupture and leads to myocardial infarction, and thrombo-inflammation, which is driven by inflammation in the vessel wall and can lead to ischaemic stroke.
![Resting platelet and collagen](/sites/default/files/styles/image_component_1_xs/public/2021-05/Understanding-molecular-mechanisms-underlying-platelet-activation--Dr-Sarah-Jones-and-Dr-Amanda-Unsworth-1.jpg?h=960b7e94&itok=pXJhn8HS)
Our research
Understanding the molecular mechanisms that underpin pathological platelet activation and occlusive thrombi formation is essential to understand the progression of cardiovascular disease and the events, which trigger blood clot formation.
Thrombosis is a multicellular process involving a range of cell types and factors within the blood and vasculature. Therapeutic strategies that target the multi-faceted nature of thrombosis could offer a multi-factorial approach to the treatment and prevention of myocardial infarction, ischaemic stroke and cardiovascular disease.
Investigating these pathological processes in different patient populations at high risk of thrombosis will enable us to identify novel antithrombotic drug targets and develop stratified approaches to preventing heart attacks and strokes in different patient populations, enabling us to develop a personalised approach to the treatment of CVD.
The British Heart Foundation and NC3Rs fund thrombosis research at Manchester Met.
British Heart Foundation-funded projects:
- Three-year project grant - Pim kinase in the regulation of platelet function, thrombosis and haemostasis
- PhD studentship - SIRT1: a novel antithrombotic target in cardiovascular disease?
- Three-year project grant – Defining the mechanisms of normal and pathological force sensing by endothelial cell adhesion complexes
NC3Rs funded grants:
- Development of E-Sense - A flexible in vitro platform to determine cardiovascular risk
- Development and characterization of a novel endothelialized in vitro model of human atherothrombosis
- Vice-Chancellor studentship - Modulation of thrombosis and antithrombotic efficacy by endothelial dysfunction
Researchers
Lead researchers
Contact
Contact us
You can contact individual members of the team through their staff profiles.
For general enquiries about the cardiovascular science research theme, you can contact theme lead Dr Fiona Wilkinson.