Mechanism of lipid accumulation in the arteries!

Mechanism of lipid accumulation in the arteries!


Scientists have identified a new potential treatment pathway for cardiovascular disease. Their research has 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.

These 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 in Science Advances, shows for the first time that levels of a protein called Tribbles-1 (TRIB1) inside macrophages controls the amount of cholesterol taken up by foam cells.

The research shows that higher levels of TRIB1 increased specific cholesterol uptake receptors, promoting arterial disease, whereas decreasing TRIB1 reduced disease. The findings of this early translational study suggest that inhibiting TRIB1 in macrophages could be a viable therapeutic target in treating cardiovascular disease.

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.

The first author of the study said: "The role of TRIB1 in macrophages has remained elusive for some time. Our research provides the missing link and highlights the importance of cell-specific expression in cardiovascular disease.

"The research into this mechanism has not yet translated into novel medical interventions. However we now have pre-clinical proof that it would be beneficial to build on this research and see which patients with cardiovascular disease would benefit from the development of treatments to manage their lipid-laden foam cell formation."

http://sciencemission.com/site/index.php?page=news&type=view&id=publications%2Fmyeloid-tribbles-1&filter=22


https://advances.sciencemag.org/content/5/10/eaax9183

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