Suggesting that Higher Levels of IGF-1 Might Slow Atherosclerosis Progression

Researchers have found that a reduced level of insulin-like growth factor 1 (IGF-1) in mice accelerates the progression of atherosclerosis, one of the more dangerous of age-related cardiovascular issues. Atherosclerosis involves the buildup of fatty deposits inside blood vessels, resulting from a cycle of damage and inflammation that starts with oxidized lipids, draws in macrophage cells that become overwhelmed and die, and creates growing plaques made up of of fats and cellular debris. The plaques narrow important blood vessels, contributing to hypertension and detrimental cardiovascular remodeling. When plaques rupture in their later stages, the result is blockage of important blood vessels that causes a stroke.

The researchers here suggest that increasing circulating IGF-1 above normal levels may slow the progression of atherosclerosis, though have yet to put together a demonstration of this, and it it isn't always the case that changes in the amount of a specific protein are mirrored in both directions. In this study, harmful effects due to lower levels of IGF-1 appear to result from reduced function of the macrophage cells responsible for clearing up damage in blood vessel walls. Other research groups have in recent years proposed enhancing macrophage capabilities to better cope with the mechanisms of atherosclerosis, but ultimately the best approach is to build some form of targeted therapy that can clear all of the damage and debris, not just somewhat improve existing systems so as to slow down its progression.

Atherosclerosis is a condition in which plaque builds up inside the arteries, which can lead to serious problems, including heart attacks, strokes or even death. Now, researchers have found that Insulin-like Growth Factor-1 (IGF-1), a protein that is naturally found in high levels among adolescents, can help prevent arteries from clogging. They say that increasing atherosclerosis patients' levels of the protein could reduce the amount of plaque buildup in their arteries, lowering their risk of heart disease. "The body already works to remove plaque from arteries through certain types of white blood cells called macrophages. However, as we age, macrophages are not able to remove plaque from the arteries as easily. Our findings suggest that increasing IGF-1 in macrophages could be the basis for new approaches to reduce clogged arteries and promote plaque stability in aging populations."

Researchers examined the arteries of mice fed a high-fat diet for eight weeks. IGF-1 was administered to one group of mice. Researchers found that the arteries of mice with higher levels of IGF-1 had significantly less plaque than mice that did not receive the protein. Since the macrophage is a key player in the development of atherosclerosis, the researchers decided to investigate potential anti-atherosclerosis effects of IGF-1 in macrophages. "We examined mice whose macrophages were unresponsive to IGF-1 and found that their arteries have more plaque buildup than normal mice. These results are consistent with the growing body of evidence that IGF-1 helps prevent plaque formation in the arteries." The researchers also found that the lack of IGF-1 action in macrophages changed the composition of the plaque, weakening its strength and making it more likely to rupture and cause a heart attack. The researchers plan to conduct the same study on larger animals before eventually studying human subjects.



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