Dr Robin N. Poston
Honorary Reader
Centre: Microvascular Research
Email: r.poston@qmul.ac.uk
Telephone: +44(0) 20 7882 3892
Profile
Robin Poston is an academic pathologist who studied Medicine at Cambridge University and the Middlesex Hospital, London, and spent many years in the Medical School at Guy’s Hospital, (now part of King’s College London). He focused on atherosclerosis research, and made the original observations indicating that adhesion molecules attract blood leukocytes to human atherosclerotic plaques.
Robert Poston is a Principal Investigator at the Centre for Microvascular Research.
Research
Binding and oxidation of LDL by the endothelium in atherosclerosis
Although the oxidation of LDL has been classically associated with macrophages, endothelial cells are also capable, and the important function of ox-LDL is in targeting and activating endothelial cells towards atherosclerotic processes. With support from the William Harvey Research Foundation, we have new evidence of the association of ox-LDL with the endothelium, in human atherosclerosis, in cultured endothelial cells, and in the periphery in an animal model of hyperlipidaemia. We wish to find the mechanisms of this oxidation, and determine its role in atherosclerosis. A research grant application is currently being submitted to the British Heart Foundation by Dr Poston and Professor Nourshargh.
CD36 inhibitors and treatment of the metabolic syndrome
Dr Poston is a co-founder of a biotech company, Arteria (France), which has developed as series of low molecular weight CD36 inhibitors. CD36 is a scavenger receptor implicated in atherosclerosis, and is also a lipid transporter involved in the induction of insulin resistance in Type II diabetes. In pre-clinical trials, these compounds have shown promise in the treatment of diabetes and atherosclerosis, and also have activity against heart failure. Clinical trials are currently being planned, and may be organised within the Barts and the London Hospital NHS Trust.
Publications
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Poston RN, Chughtai J, Ujkaj D et al. . Monocytic Cell Adhesion to Oxidised Ligands: Relevance to Cardiovascular Disease.
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Karamanavi E, McVey DG, van der Laan SW et al. (2022). The FES Gene at the 15q26 Coronary-Artery-Disease Locus Inhibits Atherosclerosis.
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Barkaway A, Rolas L, Joulia R et al. (2021). Age-related changes in the local milieu of inflamed tissues cause aberrant neutrophil trafficking and subsequent remote organ damage.
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An W, Luong LA, Bowden NP et al. (2022). Cezanne is a critical regulator of pathological arterial remodelling by targeting β-catenin signalling.
DOI: 10.1093/cvr/cvab056
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Karamanavi E, Mcvey DG, Van Der Laan SW et al. (2020). The FES gene, located at the chromosome 15Q21.6 coronary-artery-disease locus, modulates atherosclerotic plaque vulnerability.
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Heister PM, Poston RN (2020). Pharmacological hypothesis: TPC2 antagonist tetrandrine as a potential therapeutic agent for COVID‐19.
DOI: 10.1002/prp2.653
QMRO: -
Yang X, Yang W, McVey DG et al. (2020). FURIN Expression in Vascular Endothelial Cells Is Modulated by a Coronary Artery Disease–Associated Genetic Variant and Influences Monocyte Transendothelial Migration.
QMRO: -
Read JE, Luo D, Chowdhury TT et al. (2020). Magnetically responsive layer-by-layer microcapsules can be retained in cells and under flow conditions to promote local drug release without triggering ROS production.
DOI: 10.1039/c9nr10329e
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Arokiasamy S, King R, Boulaghrasse H et al. (2019). Heparanase-dependent Remodelling of Initial Lymphatic Glycocalyx 1 Regulates Tissue-fluid Drainage during Acute Inflammation in vivo.
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Poston RN (2019). Atherosclerosis: integration of its pathogenesis as a self-perpetuating propagating inflammation: a review..
QMRO:
Sponsors
Collaborators
Internal
- Professor Carol Shoulders (WHRI)
- Dr Dianne Cooper (WHRI)
- Dr Egle Solito (WHRI)
- Professor Shu Ye (WHRI)
- Professor Graham Hitman (Blizard Institute)
External
- Dr David Leake (University of Reading)