Inflammation discovery could potentially delay ageing Process: Study
The researchers believe that increasing calcium uptake by the mitochondrial macrophages could prevent harmful inflammation and its terrible effects.
Washington DC: The University of Virginia School of Medicine researchers have pinpointed a significant factor contributing to the chronic inflammation that hastens ageing.
With the help of this discovery, we may be able to turn back the hands of time and live longer, healthier lives as well as ward off age-related diseases like fatal heart disease and severe mental illnesses that rob us of our faculties.
What causes this damaging inflammation, then? Inappropriate calcium signalling in the mitochondria of some immune cells provides the solution. All cells’ mitochondria produce energy, and they heavily rely on calcium signalling.
Age-related declines in the capacity of the mitochondria in immune cells known as macrophages to take up and use calcium were discovered by UVA Health researchers under the direction of Bimal N Desai, PhD.
This, the researchers show, leads to chronic inflammation responsible for many of the ailments that afflict our later years.
The researchers believe that increasing calcium uptake by the mitochondrial macrophages could prevent harmful inflammation and its terrible effects.
Because macrophages reside in all organs of our bodies, including the brain, targeting such “tissue-resident macrophages†with appropriate drugs may allow us to slow age-associated neurodegenerative diseases.I think we have made a key conceptual breakthrough in understanding the molecular underpinnings of age-associated inflammation, said Desai, of UVAs Department of Pharmacology and UVAs Carter Immunology Center.
This discovery illuminates new therapeutic strategies to interdict the inflammatory cascades that lie at the heart of many cardiometabolic and neurodegenerative diseases. The Inflammation of Aging Inflammaging Macrophages are white blood cells that play critical roles in our immune systems and, in turn, our good health.
They swallow up dead or dying cells, allowing our bodies to remove cellular debris, and patrol for pathogens and other foreign invaders. In this latter role, they act as important sentries for our immune systems, calling for help from other immune cells as needed.
Scientists have known that macrophages become less effective with age, but it has been unclear why.
Desai and his team say their research has identified a keystone mechanism responsible for age-related changes in the macrophages.
These changes, the scientists believe, make the macrophages prone to chronic, low-grade inflammation at the best of times. And when the immune cells are confronted by an invader or tissue damage, they can become hyperactive. This drives what is known as inflammaging chronic inflammation that drives ageing.
Further, the UVA Health scientists suspect that the mechanism they have discovered will hold true not just for macrophages but for many other related immune cells generated in the bone marrow. That means we may be able to stimulate the proper functioning of those cells as well, potentially giving our immune systems a big boost in old age, when we become more susceptible to disease.
Fixing inflammaging won’t be as simple as taking a calcium supplement. The problem isn’t a shortage of calcium so much as the macrophages inability to use it properly. But Desai’s new discovery has pinpointed the precise molecular machinery involved in this process, so we should be able to discover ways to stimulate this machinery in ageing cells.
This highly interdisciplinary research effort, at the interface of computational biology, immunology, cell biology and biophysics, wouldn’t have been possible without the determination of Phil Seegren, the graduate student who spearheaded this ambitious project, Desai said.
Now, moving forward, we need an equally ambitious effort to figure out the wiring that controls this mitochondrial process in different types of macrophages and then manipulate that wiring in creative ways for biomedical impact.
