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Humanity has long been intrigued by how we age gracefully and whether we may take any steps to slow down the process. But despite ongoing research, the solution to how we might effectively fight aging is still a mystery.
Researchers at the University of Glasgow and the Mayo Clinic in the United States have now uncovered some of the basic mysteries underlying the aging process, providing a potential new target for therapy.
The article, “Apoptotic stress causes mtDNA release during senescence and drives the SASP,” was written and published in Nature. It looks into how inflammation is brought on by aging and damaged cells and how to stop it in order to promote healthy aging and even enhance the treatment of conditions like cancer.
Our cells create inflammatory proteins as we age, which accelerates the aging process. By destroying cells, cancer treatments can trigger this similar inflammatory process, which might hinder the effectiveness of treatments in patients.
The School of Cancer Sciences’ Professor Stephen Tait and his team-led new study reveals that the energy-producing organelles known as mitochondria have a significant inflammatory function in human cells.
The researchers discovered that mitochondria become leaky in aged cells or after cancer therapy, releasing DNA that encourages inflammation and, as a result, aging. The scientists later determined that if they could stop the mitochondria from leaking, this would stop inflammation and enhance health during aging.
Their finding shows that inhibiting mitochondrial-driven inflammation may provide a novel strategy for promoting healthy aging and enhancing the effectiveness of cancer treatments.
The research demonstrates a completely unanticipated connection between mitochondria and the inflammatory effects of aging cells, according to Professor Stephen Tait. They discover that in aging and injured cells, mitochondrial permeabilization—a procedure intrinsically associated with cell death—promotes inflammation. This opens up new research fields with the exciting possibility of bringing new cancer and aging therapeutic products to market.
Sources:
Stella Victorelli et al. (2023). Apoptotic stress causes mtDNA release during senescence and drives the SASP, Nature. DOI: 10.1038/s41586-023-06621-4
https://phys.org/news/2023-10-scientists-biological-secrets-aging.html
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