Title: From mummies, through sponges, and to inflammation – searching for novel biomarkers and treatments to prevent heart disease and stroke.

Abstract: I will discuss how work in my lab over the last sixteen years has led to us identifying key inflammatory cell subpopulations which drive the development of atherosclerosis, the underlying cause of heart attacks, stroke, and peripheral arterial disease. I will cover the mechanistic insight within these subpopulations that has resulted in the detection of several novel therapeutic targets, and provide key proof-of-principle in vivo data that supports the pursuance of several molecules as future therapeutics.

Biography: Professor Jason Johnson is a past-holder of a British Heart Foundation Senior Research Fellowship and leads the Laboratory of Cardiovascular Pathology at the University of Bristol.

He has a long-standing interest in the pathophysiology of numerous cardiovascular pathologies including atherosclerosis, aortic aneurysms, and restenosis. His studies include a marriage of basic science and translational cardiovascular research with the goal of facilitating the development and deployment of novel therapies to combat the aforementioned cardiovascular diseases, alongside the identification of potential biomarkers of disease progression.

Since gaining his PhD in 2005, Professor Johnson’s research has underpinned the dogma that not all matrix metalloproteinases (MMPs) play detrimental roles in atherosclerotic plaque progression. Moreover, he has aided the identification of a macrophage phenotype (under the control of GM-CSF) which is characterised by high MMP-12 and MMP-14 protein expression alongside low TIMP-3 levels. Further work has also identified a novel node of microRNA regulation within GM-CSF macrophages, highlighting several potential new therapeutic avenues, including miR-181b inhibition and the selective inhibition of MMP-12. Collectively, these studies have made a major contribution to understanding the role of matrix metalloproteinases and macrophage heterogeneity in atherosclerotic plaque progression. Supporting studies in human aneurysm samples and pertinent pre-clinical in vivo models has reaffirmed the notion that the proteolytic profile of macrophage subsets predicts aneurysm development and progression. These findings are now being tested in a novel ex vivo human model of aneurysm that will hopefully supplant the requirement for animal studies. Recent new therapies and biomarkers for atherosclerosis and related pathologies are now being explored through industrial collaborations.

All welcome

In OS6 Oakfield House or zoom