Inflammation Linked to Calcium Signaling in Immune Cells

A new study from University of Virginia School of Medicine researchers reveals that improper calcium signaling in the mitochondria of macrophages is a crucial driver of chronic inflammation, which accelerates aging and leads to various ailments later in life.

Led by Bimal N. Desai, the UVA Health researchers found that as macrophages age, their ability to absorb and utilize calcium declines. This impairment results in persistent inflammation responsible for many age-related health issues. However, the team believes that enhancing calcium uptake in these mitochondria could counteract harmful inflammation and its effects. By targeting "tissue-resident macrophages" with suitable medications, age-associated neurodegenerative diseases might be slowed down.

The discovery, published in Nature Aging, sheds light on the molecular basis of age-associated inflammation, offering new therapeutic strategies to address cardiometabolic and neurodegenerative diseases. Macrophages, crucial white blood cells in the immune system, play essential roles in maintaining good health by clearing out cellular debris and responding to pathogens. The research indicates that age-related changes in macrophages make them susceptible to chronic inflammation, leading to "inflammaging"—a chronic inflammatory state that contributes to aging.

The researchers suspect that this keystone mechanism may also apply to other immune cells produced in the bone marrow, potentially providing a significant boost to the immune system in old age when susceptibility to diseases increases.