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New Potential Treatment for Atherosclerosis Identified


A team of researchers from the University of Sheffield in the UK has identified a protein that plays a key role in the development of atherosclerosis, the leading cause of death worldwide.

The trouble with Tribbles 1

Researchers have demonstrated for the first time that the protein known as Tribbles 1 (TRIB1) is expressed by macrophages that are linked to the formation of the plaques that clog our arteries and eventually kill us. Macrophages are responsible for removing cellular garbage and other waste from our bodies to keep us healthy, and that includes the insides of our arteries.

These garbage gobblers patrol our bloodstream, and when they detect fatty deposits lodged in the walls of our blood vessels, they move in to clean them up by absorbing the cholesterol and transporting it away.

Unfortunately, macrophages are not great at processing some forms of cholesterol and can become overwhelmed when they try to absorb too much. Macrophages that absorb large quantities of these fatty deposits become bloated, cholesterol-laden cells known as foam cells, which become trapped in the wall of the artery and can do little more than generate inflammation and summon more macrophages to the site.

These new macrophages also become trapped after trying to absorb the fatty deposits and become overwhelmed and die. Thus, the injury site gradually becomes a macrophage graveyard, and the dead and dying foam cells form the basis of the familiar arterial plaques that accompany atherosclerosis.

The new study shows that TRIB1 regulates the amount of cholesterol taken up by foam cells. The researchers showed that the higher the level of TRIB1 present in the bloodstream, the more cholesterol the foam cells uptake, which encourages atherosclerosis to develop. They also showed that by decreasing the presence of TRIB1, disease progression was reversed.

Macrophages drive atherosclerotic plaque progression and rupture; hence, attenuating their atherosclerosis-inducing properties holds promise for reducing coronary heart disease (CHD). Recent studies in mouse models have demonstrated that Tribbles 1 (Trib1) regulates macrophage phenotype and shows that Trib1 deficiency increases plasma cholesterol and triglyceride levels, suggesting that reduced TRIB1 expression mediates the strong genetic association between the TRIB1 locus and increased CHD risk in man. However, we report here that myeloid-specific Trib1 (mTrib1) deficiency reduces early atheroma formation and that mTrib1 transgene expression increases atherogenesis. Mechanistically, mTrib1 increased macrophage lipid accumulation and the expression of a critical receptor (OLR1), promoting oxidized low-density lipoprotein uptake and the formation of lipid-laden foam cells. As TRIB1 and OLR1 RNA levels were also strongly correlated in human macrophages, we suggest that a conserved, TRIB1-mediated mechanism drives foam cell formation in atherosclerotic plaque and that inhibiting mTRIB1 could be used therapeutically to reduce CHD.


This research is still in its initial stages, but this serves as good preclinical evidence that targeting this protein to manage cholesterol-laden foam cells could be a viable way to prevent or reverse atherosclerosis.

If these researchers can find a way to block or reduce the activity of TRIB1, it could form the basis of a therapy to prevent the formation of bloated foam cells and atherosclerotic plaques and allow the macrophages to clean away the waste without themselves becoming trapped. In other words, it could offer a solution to atherosclerosis and a way to clean out clogged blood vessels.

This is not the only approach currently being developed to tackle the root cause of atherosclerosis. Repair Biotechnologies is also working on an approach that could improve how macrophages break down cholesterol, making them more robust and able to remove it more effectively. The company’s founder, Reason, gave a talk about his company at our conference earlier this year.

SENS Research Foundation has also been busy developing an approach that works by removing a particularly toxic form of oxidized lipid known as 7-ketocholesterol directly from the macrophages, and we should have some exciting news about this soon.

A world without atherosclerosis and its resulting heart attacks and strokes cannot come soon enough, given that this disease is the world’s leading cause of death.

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[1] Johnston, J. M., Angyal, A., Bauer, R. C., Hamby, S., Suvarna, S. K., Baidžajevas, K., … & Goodall, A. H. (2019). Myeloid Tribbles 1 induces early atherosclerosis via enhanced foam cell expansion. bioRxiv, 615872.

About the author

Steve Hill

Steve serves on the LEAF Board of Directors and is the Editor in Chief, coordinating the daily news articles and social media content of the organization. He is an active journalist in the aging research and biotechnology field and has to date written over 600 articles on the topic, interviewed over 100 of the leading researchers in the field, hosted livestream events focused on aging, as well as attending various medical industry conferences. His work has been featured in H+ magazine, Psychology Today, Singularity Weblog, Standpoint Magazine, Swiss Monthly, Keep me Prime, and New Economy Magazine. Steve is one of three recipients of the 2020 H+ Innovator Award and shares this honour with Mirko Ranieri – Google AR and Dinorah Delfin – Immortalists Magazine. The H+ Innovator Award looks into our community and acknowledges ideas and projects that encourage social change, achieve scientific accomplishments, technological advances, philosophical and intellectual visions, author unique narratives, build fascinating artistic ventures, and develop products that bridge gaps and help us to achieve transhumanist goals. Steve has a background in project management and administration which has helped him to build a united team for effective fundraising and content creation, while his additional knowledge of biology and statistical data analysis allows him to carefully assess and coordinate the scientific groups involved in the project.
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