CHARLOTTESVILLE, Va. — Researchers have uncovered a significant factor behind chronic inflammation, known to speed up the aging process. This breakthrough could potentially pave the way for us to “slow the clock,” ensuring longer, healthier lives, and offering solutions to prevent conditions like heart diseases and brain disorders linked with aging.
The culprit behind this detrimental inflammation lies in incorrect calcium signaling in the mitochondria, the energy-producing structures within cells of certain immune cells. For context, mitochondria are akin to power generators in every cell, and they heavily depend on calcium signaling for their function.
Researchers from the University of Virginia revealed that as we age, the mitochondria in immune cells called macrophages reduce their capacity to absorb and utilize calcium. This reduction is a significant contributor to the chronic inflammation observed in our senior years.
By enhancing the calcium uptake of these mitochondrial macrophages, it may be possible to curb this harmful inflammation. Macrophages, present in all our organs, including the brain, are prime targets. Thus, employing specific drugs to target these “tissue-resident macrophages” might be a potential strategy to deter age-related neurodegenerative diseases.
“I think we have made a key conceptual breakthrough in understanding the molecular underpinnings of age-associated inflammation,” says Dr. Bimal N. Desai, of UVA’s Department of Pharmacology and UVA’s Carter Immunology Center, in a university release. “This discovery illuminates new therapeutic strategies to interdict the inflammatory cascades that lie at the heart of many cardiometabolic and neurodegenerative diseases.”
Macrophages are essentially white blood cells that play a pivotal role in our immune systems. They help in removing cellular debris by consuming dead or dying cells and also act as immune sentinels, guarding against pathogens and other external threats. Although scientists have recognized that macrophages’ efficiency declines with age, the reason remained elusive until Dr. Desai’s recent findings.
The team at UVA Health believes they’ve pinpointed a central mechanism causing age-related shifts in macrophages. These alterations render macrophages susceptible to constant, mild inflammation. When these immune cells encounter threats or tissue harm, they can overreact, leading to “inflammaging” – the chronic inflammation associated with aging.
The mechanism identified might apply not only to macrophages but to other similar immune cells produced in the bone marrow. This indicates the potential of enhancing the performance of these cells, giving our immune systems a valuable boost during old age when vulnerability to diseases increases.
However, addressing “inflammaging” isn’t as straightforward as merely consuming calcium supplements. The core issue is the macrophages’ diminished capacity to utilize calcium effectively. These findings have identified the exact molecular mechanism at play, opening the door for potential solutions to stimulate aging cells.
The next phase requires a comprehensive effort to comprehend and potentially manipulate this mitochondrial process in different macrophage types for tangible health benefits.
The study was published in the journal Nature Aging.
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