The “thread” of aging is beginning to be unraveled by researchers at the University of Virginia School of Medicine who have discovered a key factor in chronic inflammation, which accelerates aging. Their finding could allow us to turn back time and live longer, healthier lives, and may even allow us to prevent age-related diseases such as heart disease and brain disorders that “steal” our abilities us.
So what determines this harmful inflammation? Inappropriate calcium signaling in the mitochondria of certain cells of the immune system. Mitochondria are the energy generators of cells and rely mainly on calcium signaling.
UVA Health researchers led by Bimal N. Desai found that mitochondria in immune cells called macrophages lose their ability to take up and use calcium with the passage of age. This, as the researchers show, leads to chronic inflammation that is responsible for many of the ailments that afflict us in old age.
In their related study titled “Reduced mitochondrial calcium uptake in macrophages is a major driver of inflammaging” published in Nature Aging, the researchers believe that increasing calcium uptake by macrophage mitochondria could prevent inflammation and its dire effects. Because macrophages are found in all organs of our body, including the brain, targeting the macrophages that “reside” there with appropriate drugs may allow us to slow age-related neurodegenerative diseases.
The inflammation of aging
Macrophages are white blood cells that play a critical role in our immune system and good health. They ingest dead cells, allowing our bodies to remove cellular debris and patrol for pathogens and other foreign invaders. In this latter role, they act as important sentinels for our immune system, calling other immune cells to help.
Scientists knew that macrophages become less efficient with age, but it wasn’t clear why. Desai’s new discovery points to the answers.
Desai and his team say their research has identified a “key” mechanism responsible for age-related changes in macrophages. These changes, the scientists believe, make macrophages susceptible to chronic, low-grade inflammation at best. And when immune cells are confronted with an invader or tissue damage, they can go into overdrive. But this is the chronic inflammation that leads to aging.
In addition, the UVA Health scientists suspect that the mechanism they discovered will apply not only to macrophages but also to many other related immune cells that are created in the bone marrow. This means we may be able to stimulate the proper functioning of these cells as well, potentially giving our immune system a big boost in old age, when we become more susceptible to disease.
Next steps
Correcting “inflammatory aging” is not expected to be as simple as taking a calcium supplement. The problem is not the lack of calcium, but the inability of the macrophages to use it properly. But this new discovery by Desai has highlighted the exact molecular mechanism involved in this process, so we should be able to discover ways to enhance the mechanism of calcium utilization by aging cells.
