Inflammation discovery offers hope for age-related diseases
Researchers have made a significant breakthrough in the field of ageing research, uncovering a key driver of chronic inflammation that accelerates the ageing process.
Published in Nature Aging, researchers at the University of Virginia School of Medicine have made a significant breakthrough in the field of aging research, uncovering a key driver of chronic inflammation that accelerates the aging process. This finding holds the promise of potentially slowing down the aging clock, allowing individuals to lead longer, healthier lives, while also providing potential avenues to prevent age-related conditions, such as heart disease and neurodegenerative disorders.
The culprit: improper calcium signalling in mitochondria
The research led by Bimal N. Desai, PhD, sheds light on the role of mitochondria. Mitochondria generate almost all our energy in the form of ATP, 1 they are considered the powerhouses of cells, and their reliance on calcium signalling. Specifically, the team found that as immune cells called macrophages age, their ability to take up and utilise calcium declines. This impairment in calcium signalling leads to chronic inflammation, which is associated with a host of age-related ailments.
Targeting inflammation to improve health span
The researchers propose that increasing calcium uptake in mitochondrial macrophages could be a promising approach to prevent harmful inflammation and its detrimental effects.
This impairment in calcium signalling leads to chronic inflammation, which is associated with a host of age-related ailments.
As macrophages are present in all organs, including the brain, targeting these “tissue-resident macrophages” with appropriate drugs may offer a way to slow down age-related neurodegenerative diseases.
Revealing the mechanisms of inflammageing
Macrophages play crucial roles in the immune system, engulfing dying cells and detecting foreign invaders. However, with age, these immune cells become less effective. Desai’s team has now identified a “keystone” mechanism responsible for age-related changes in macrophages. These changes make the macrophages prone to chronic, low-grade inflammation even without external triggers. When faced with an invader or tissue damage, the immune cells become hyperactive, driving a phenomenon known as “inflammageing.”
Expanding the impact of the discovery
The researchers suspect that the mechanism they uncovered may extend to other immune cells generated in the bone marrow. This raises the exciting possibility of stimulating the proper functioning of these immune cells as well, bolstering the immune system’s resilience in old age when susceptibility to diseases increases.
Challenges and future prospects
While addressing “inflammageing” will not be as straightforward as taking a calcium supplement, Desai’s discovery has pinpointed the specific molecular machinery involved in this process. This paves the way for exploring ways to stimulate this machinery in aging cells, potentially offering new avenues for therapeutics.
An ambitious research journey
The interdisciplinary nature of this research, combining computational biology, immunology, cell biology, and biophysics, was instrumental in its success. Phil Seegren, the graduate student leading this ambitious project, played a pivotal role. Moving forward, the team aims to decipher the regulatory wiring controlling this mitochondrial process in various macrophage types, paving the way for innovative strategies to positively impact human health.
The University of Virginia’s inflammation discovery opens exciting possibilities for slowing the aging process and preventing age-related diseases. By homing in on the role of calcium signalling in immune cells, researchers are now better equipped to explore potential therapeutic interventions that may transform the landscape of aging research and improve health span worldwide.
- Lane N. Power, sex, suicide: Mitochondria and the meaning of life. Oxford, United Kingdom: Oxford University Press; 2018.