Cardiovascular disease (CVD) kills about 480 people every day in the UK – it is the leading cause of death in men and second leading cause of death in women. Atherosclerosis underpins most cardiovascular disease by causing a build-up of lipid (fat) which narrows the arteries leading to heart attacks. Despite the availability of medications to limit cholesterol and blood pressure levels, and devices to widen arteries, atherosclerosis causes significant morbidity and mortality and better treatments are needed. The immune system has emerged as an integral part of our circulatory system and as such it pays a role in CVD. Thus, there is a growing interest in treating atherosclerosis with anti-inflammatory drugs, but by affecting the whole body they could leave patients more susceptible to infection. Creating anti-inflammatory therapies specifically targeted to the atherosclerotic plaque would minimise this side effect.
Our innate immune system has the helpful ability to trigger inflammation in response to infection and injury. In atherosclerosis, innate immune cells like macrophages become chronically activated by excess lipid and damage the artery walls. Toll-like receptors (TLRs) on the surface of macrophages are involved in this detrimental process, constantly recognising lipoproteins and triggering inflammation. Together this suggests that therapies to target macrophages and other cells in the atherosclerotic plaque could be powerful weapons to treat atherosclerosis. However, more knowledge about the molecular immunology of cardiovascular disease is needed to guide the design of future therapies.
A new programme grant, funded by the British Heart Foundation and led by Professor Claudia Monaco at the Kennedy Institute of Rheumatology in Oxford, aims to unpick the inflammatory processes of lipid-driven inflammation in atherosclerosis and to define the role of TLRs in more detail. This could lead to better therapies targeting the innate immune system.
Read the full story on the Kennedy Institute website.