Posted on 01/02/2026 4:05:51 PM PST by ConservativeMind
Two complementary studies reveal how an insufficient supply of energy in macrophages, key immune cells in artery walls, drives the progression of atherosclerosis—and how this knowledge could lead to better diagnostics and future therapies.
Atherosclerosis—the buildup of fatty plaques inside arteries—is the leading cause of heart attacks and strokes worldwide. Although the role of cholesterol in plaque formation has long been a focus, scientists increasingly recognize that the immune system plays a decisive role in determining whether plaques remain stable or become unstable and thus prone to rupture, which can lead to heart attacks or strokes.
In two newly published studies, researchers showed that poor availability of the amino acid glutamine in macrophages can determine the worsening of artery plaques. The researchers also identified new ways to detect dangerous plaques.
Macrophages are the body's clean-up crew. Inside artery plaques, they ingest fats, remove dying cells, and help repair damaged tissue. But to perform these protective tasks, macrophages require energy.
In the first study, the researchers discovered that macrophages rely heavily on glutamine uptake from their environment to fuel their restorative functions. A specific transporter protein, SLC7A7, acts as a gateway that allows glutamine to enter the cell. When this gateway is blocked, macrophages lose energy and perform poorly, resulting in plaques that are larger and more unstable, which is a known risk factor for heart attacks and strokes in people.
Reduced activity of this pathway was linked to more dangerous plaque features also in human artery samples.
The second study builds on this biological insight and moves toward the clinic. By studying macrophages with advanced single-cell technologies, the researchers identified protein markers such as TREM2, FOLR2, and SLC7A7 that highlight high-risk plaques.
Based on these, PET imaging could be used to detect inflammatory plaque activity rather than just the size.
(Excerpt) Read more at medicalxpress.com ...
For some reason, our ability to properly get or use it is lessened, from a transporter protein called SLC7A7, and this shows up as a lack of energy for key cells that clean up arterial plaques, so the plaques grow.
From some searching I did:
“While specific activators are unknown, maintaining normal cellular function—such as balanced amino acid levels and metabolic health—may support proper SLC7A7 expression.”
The role of glutamine had not been understood as needed for these clean up processes.
New!
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