Some researchers have discovered how the cells that make us age work. And (maybe) how to stop them: here’s what to know
For now it is just a study, but a very ambitious one: understanding how to govern one of the secret mechanisms of aging. A group of scientists fromGraduate University of Okinawa Institute of Science and Technology (OIST) has in fact discovered that damaged cells do not always die, but continue to act with sometimes even harmful effects on our body. And getting to the bottom of this mechanism could be an important step forward in addressing aging, disease and healing processes. But how exactly does it work?
Cellular aging
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Premise: cells are protected by a cell membranea delicate and flexible barrier only 5 nanometers thick (about 1/20 the thickness of a soap bubble, ed). It acts like a shield, allowing certain substances in and out while keeping others out. But the membrane is vulnerable to damage resulting from daily activities, such as muscle contractions and injuries. Some of this damage is repairable, some is not. Japanese researchers say that although cells have mechanisms to repair minor damage, when they fail to do so, they either die or enter a state of senescence, meaning they stop dividing but remain metabolically active, contributing to various physiological processes, both beneficial and harmful. “When I started this project, I simply aimed to understand the repair mechanisms of the damaged cell membrane,” explains Keiko Kono, head of the Membranology unit and senior author of the study published in Nature. “Unexpectedly, we discovered that damage to the cell membrane, in a certain sense, changes the fate of cells.”
Cellular senescence
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The team of scientists analyzed how the damage to plasma membrane would influence the aging of human cellsusing lung fibroblasts and skin grown in the laboratory. For damage the researchers used detergents, bacterial toxins and lasers on the membranes. The cells thus entered a state of senescence, activating different genetic programs compared to cells aged due to DNA mutations: one of these involved, for example, their contribution to wound healing, which is undoubtedly useful. But Senescent cells also produce proteins that can modify immune responses, influencing everything from cancer to the aging process itself. For this reason, the presence of senescent cells in the body and their role in health and disease are the subject of many studies, some of which suggest that their removal could rejuvenate bodily functions.
But that’s not all: until now, scientists believed that cellular senescence was triggered by repeated cell divisions or other stresses, such as DNA damage. The new study highlights a different pathway that would also involve calcium ions and the tumor suppressor gene p53, caused by damage to the cell membrane. A discovery which, if confirmed, could contribute to the development of a targeted treatment strategy and increase human longevity, allowing “old” cells to perform a useful function without causing damage to the organism.
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