Protein link in circulation disease treatment

RESEARCHERS AT the University of Sheffield have identified a new potential treatment pathway for cardiovascular disease.

Studies have shown for the first time that a protein expressed in a subset of immune cells contributes towards the build-up of fatty deposits in arteries, which leads to cardiovascular disease.

Diseases of the heart and circulatory system involve narrowed or blocked blood vessels and can lead to a range of conditions, including heart attacks, strokes and vascular dementia.

They cause 27 per cent of deaths in England and some 670,000 people in Yorkshire and the Humber are living with cardiovascular disease, according to the British Heart Foundation.

The fatty deposits are caused by macrophages, a subset of immune cells known to take up surplus cholesterol.

When this is present in excess, they mature into larger cholesterol-laden cells known as foam cells which accumulate and cause blockages inside arteries.

The study, published today in Science Advances, shows for the first time that levels of a protein called Tribbles-1 (TRIB1) inside macrophages control the amount of cholesterol taken up by foam cells. Higher levels of TRIB1 increased specific cholesterol uptake receptors, promoting arterial disease, whereas decreasing TRIB1 reduced disease, the research shows.

The findings of the study, which also involved the University of Leicester and scientists from Hungary and the US, suggest that inhibiting TRIB1 in macrophages could be a viable therapeutic target in treating cardiovascular disease in the future.

Researchers have long been trying to identify the proteins regulated by TRIB1 to understand their effects, and whether they are of benefit or are detrimental to disease development.

Dr Jessica Johnston, of the University of Sheffield, said the research had provided the “missing link” to the elusive role played by TRIB1 in macrophages.