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Although recent years have seen a revolution in the prevention and treatment of heart attack and stroke, these remain the biggest causes of death and disability worldwide. They are caused by a process known as atherosclerosis, which involves progressive narrowing – and eventually complete blockage – of arteries supplying blood to the heart and brain. It has long been known that accumulation of cholesterol in the blood vessel wall is a major factor in this disease, and drugs such as statins which lower blood cholesterol have revolutionised the treatment of cardiovascular disease. Nonetheless, despite the success of such treatments, heart attack and stroke continue to exert a huge health and economic burden, and recent evidence suggests that this residual risk is likely explained in large part by inflammation within the arterial wall. Our group’s research is focussed on how platelets and leukocytes (white blood cells), circulating blood cells which are normally involved in clotting and fighting off infection respectively, are involved in the initiation and progression of atherosclerosis through promoting inflammation. A better understanding of how atherosclerosis develops, including the role of inflammation in this, will allow new treatments to be developed, and this is the ultimate goal of our research.

People

Albert  Ferro

Professor of Cardiovascular Clinical Pharmacology

Projects

Ferro lab project 1 atherosclerosis
CXCR2 inhibition as a novel treatment of atherosclerosis

There is emerging evidence of the central role of neutrophils in both atherosclerotic plaque formation and rupture. Patients with lower neutrophil counts following acute coronary syndromes tend to have a greater coronary flow reserve, which is a strong predictor of long-term cardiovascular health. But so far, no data are available regarding the impact of neutrophil inhibition on cardiovascular clinical or surrogate endpoints. We are undertaking a clinical trial is to investigate the effects of AZD5069, a cysteine-X-cysteine chemokine receptor 2 (CXCR2) inhibitor, on coronary flow reserve and coronary structure and function in patients with coronary artery disease.

    Ferro lab project 2
    The role of netrin-1 in cardiovascular physiology and atherosclerosis

    The netrins form a family of laminin-related proteins which were first described as modulators of cell migration and axonal guidance during fetal development. Netrin-1 is involved in the regulation of angiogenesis, organogenesis, cancer and inflammation. An NF-κB-dependent truncated isoform of netrin-1 has also been shown to be produced in endothelial and some types of cancer cells. Recent evidence from our lab and others suggests that the two isoforms of netrin-1 have important roles in modulating monocyte / macrophage recruitment in the arterial wall, and our lab is exploring the precise roles of these isoforms in the natural history of atherosclerosis.

      Ferro lab project 3 platelets
      Novel blood biomarkers of atherosclerosis

      Recent evidence has shown that inflammation plays a crucial part in the pathophysiology of atherosclerosis. Monocytes / macrophages are an integral part of this inflammatory response, and evidence from our lab demonstrates that monocytes undergo transformation to a more pro-inflammatory phenotype, triggered by their association with platelets, in patients with underlying cardiovascular risk factors. We are now undertaking detailed proteomic and phenotypic analyses of monocytes in patients from our cardiovascular risk clinics, with a view not only to better understanding the pathophysiological role played by monocytes in atherogenesis but also to better predicting which patients are likely to have underlying hitherto clinically silent atherosclerotic disease.

        Publications

          Awards

          AstraZeneca investigator-led grant: CXCR2 inhibition: a novel approach to treating coronary heart disease. £1,250,000.

          British Heart Foundation PhD studentship (for Vasco Claro): Netrin-1 and macrophage phenotype: role in the pathophysiology of atherosclerosis. £119,498.

          University of Kuwait scholarship and PhD studentship (for Dr Fatemah Almarri): Circulating monocyte phenotype: a novel biomarker for atherosclerosis. £157,740.

          People

          Albert  Ferro

          Professor of Cardiovascular Clinical Pharmacology

          Projects

          Ferro lab project 1 atherosclerosis
          CXCR2 inhibition as a novel treatment of atherosclerosis

          There is emerging evidence of the central role of neutrophils in both atherosclerotic plaque formation and rupture. Patients with lower neutrophil counts following acute coronary syndromes tend to have a greater coronary flow reserve, which is a strong predictor of long-term cardiovascular health. But so far, no data are available regarding the impact of neutrophil inhibition on cardiovascular clinical or surrogate endpoints. We are undertaking a clinical trial is to investigate the effects of AZD5069, a cysteine-X-cysteine chemokine receptor 2 (CXCR2) inhibitor, on coronary flow reserve and coronary structure and function in patients with coronary artery disease.

            Ferro lab project 2
            The role of netrin-1 in cardiovascular physiology and atherosclerosis

            The netrins form a family of laminin-related proteins which were first described as modulators of cell migration and axonal guidance during fetal development. Netrin-1 is involved in the regulation of angiogenesis, organogenesis, cancer and inflammation. An NF-κB-dependent truncated isoform of netrin-1 has also been shown to be produced in endothelial and some types of cancer cells. Recent evidence from our lab and others suggests that the two isoforms of netrin-1 have important roles in modulating monocyte / macrophage recruitment in the arterial wall, and our lab is exploring the precise roles of these isoforms in the natural history of atherosclerosis.

              Ferro lab project 3 platelets
              Novel blood biomarkers of atherosclerosis

              Recent evidence has shown that inflammation plays a crucial part in the pathophysiology of atherosclerosis. Monocytes / macrophages are an integral part of this inflammatory response, and evidence from our lab demonstrates that monocytes undergo transformation to a more pro-inflammatory phenotype, triggered by their association with platelets, in patients with underlying cardiovascular risk factors. We are now undertaking detailed proteomic and phenotypic analyses of monocytes in patients from our cardiovascular risk clinics, with a view not only to better understanding the pathophysiological role played by monocytes in atherogenesis but also to better predicting which patients are likely to have underlying hitherto clinically silent atherosclerotic disease.

                Publications

                  Awards

                  AstraZeneca investigator-led grant: CXCR2 inhibition: a novel approach to treating coronary heart disease. £1,250,000.

                  British Heart Foundation PhD studentship (for Vasco Claro): Netrin-1 and macrophage phenotype: role in the pathophysiology of atherosclerosis. £119,498.

                  University of Kuwait scholarship and PhD studentship (for Dr Fatemah Almarri): Circulating monocyte phenotype: a novel biomarker for atherosclerosis. £157,740.

                  PhD Students

                  Our Partners

                  Our research is funded by the British Heart Foundation, Kuwait University and AstraZeneca plc.

                  BHF

                  British Heart Foundation

                  AstraZeneca partner logo

                  AstraZeneca

                  Kuwait university logo

                  Kuwait University

                  Group lead

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