Heart attack, here is the “scavenger” enzyme of the arteries that will tell who is most at risk

Heart attack, here is the “scavenger” enzyme of the arteries that will tell who is most at risk

It’s a real waterfall. Difficult to arrest. Because when the plaque breaks on the wall of the coronary artery, its contents flow out into the vessel. And it creates a series of events that ultimately lead to blockage of blood circulation. Thus was bornheart attack. And, similarly, if the rupture occurs in an artery that supplies the brain, the risk is called stroke.

Finding out why one plaque is more “friable” than others and above all how to create a sort of “cement” that reduces the risk of rupture is one of the great challenges of cardiology. But basic research, which will perhaps bring results in the future, is discovering a series of mechanisms which on the one hand could indicate who has a plaque at greater risk of rupture, and on the other propose treatments with specific antibodies which fix these concretions along The vase.

The key to everything lies in a protein, called TREM2. Discovering the role of this protein which acts like a “garbage collector” by cleaning up the plaque and keeping it more robust and less prone to breaking is a research which has seen protagonists Christoph Binder And Florentina Porsch of the University of Vienna together with Clément Cochain, Alma Zernecke And Marie Piollet of the University Hospital of Würzburg. The study appeared on Nature Cardiovascular Research and opens the way to early diagnosis of those who may be having a heart attack and even to targeted therapies to stabilize the plaque.

The secret of the “scavenger” protein

The study revolves around the role of macrophages. These specific white blood cells basically have the task of incorporating waste, as happens with particles of bad cholesterol or LDL. In practice, therefore, macrophages accumulate these lipoproteins and transform into foam cells, rich in cholesterol, which form the base of the plaque.

But why are there plaques that break, causing a heart attack, and others that remain stable? According to scholars, everything is linked to the TREM2 protein (Triggering Receptor Expressed on Myeloid Cells – 2) which controls the activity of the macrophages themselves. In particular, the protein regulates the survival of the so-called foam cells, particularly common in atherosclerotic plaques, and promotes the elimination of damaged or dying cells. In practice, it cleans the plaque of waste. And therefore it keeps it “cleaner” and stable, reducing the risk of heart attack. But not only that: TREM2 could become the target of a specific therapy for the prevention of heart attack.

Treating animals predisposed to developing atherosclerosis with a specific antibody against TREM2 reduced the formation of unstable plaques. Again: by studying this protein, we could also predict future risk. In fact, it has been seen that there is a relationship between a soluble form of this protein (“sTREM2”) and the progression ofatherosclerosis. In short: TREM2 could prove to be a target for drugs and a biomarker for those at greatest risk, allowing preventive efforts to be concentrated.

Towards prevention and tailored therapies

We are only at the beginning. But the study opens up truly important horizons for the optimal control of atherosclerosis lesions. “The role of TREM2 seems to be a real opportunity in the diagnosis and treatment of our cardiovascular patients – he confirms Stefano Carugo, Director of the Cardio-thoracic-vascular Department of the Irccs Policlinico di Milano – University of Milan. In fact, the reasons why an atherosclerotic plaque not only forms but can also evolve towards its instability are not always clear. The inflammatory process, especially when not adequately counteracted, certainly plays a role of primary importance.”

The knowledge opened up by research goes in this direction. Indeed, TREM2 deficiency appears to be important in the progression not only of inflammation, but also of atherosclerotic plaque. All this, through the demonstrated “cleaning” action of the vessels from the cells that now need to be eliminated. “This brilliant study can therefore open a new frontier in the management of atherosclerotic patients and consequently in the importance of measuring TREM2 – concludes Carugo. Its deficiency can classify our patients as more at risk of heart attack and stroke and therefore place them under greater attention in terms of reducing the lipid profile and active action against inflammatory processes”.

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