Damage to cell membranes drives cell aging, according to a recent study. Our cells are enclosed by a thin membrane that is only 5 nanometers thick, or 1/20 of a soap bubble. Physiological processes such as muscular contraction and tissue injury can easily cause cell damage. To deal with such damage, cells have systems that can repair membrane damage to a limited extent.
Damage to cell membranes drives cell aging, A detailed Research
Previously, mechanical injury to the cell membrane was thought to result in just two possible biological outcomes: recuperation or death. In a current study, however, researchers discovered a third outcome: cellular senescence. The work appears in Nature Aging.
“When I started this project, I simply wanted to understand the repair mechanisms of damaged cell membranes,” recalls Professor Keiko Kono, head of the Okinawa Institute of Science and Technology Membranology unit and senior author of the study, which included multiple members of the unit, including Kojiro Suda, Yohsuke Moriyama, Nurhanani Razali, and colleagues. “Unexpectedly, we ended up discovering that cell membrane damage, in a sense, switches cell fate.”
The degree of injury and subsequent calcium ion influx are critical factors in determining cell fate. The thin cell membrane injury is easily repaired, allowing the cells to divide normally. The highest level of cell membrane damage causes cell death.
Cancer cells divide indefinitely. Non-cancerous normal cells, on the other hand, have a limited ability to divide—around 50 times before division is irrevocably stopped and the cells enter a state known as cellular senescence. Senescent cells remain metabolically active, but unlike young and healthy cells, they release a variety of secretory proteins that stimulate immunological responses in both surrounding tissues and distant organs. This system can cause both positive and unfavorable changes in our bodies, such as accelerated wound healing, cancer promotion, and aging.
Several research over the last decade have found that senescent cells occur in animal bodies, including humans, and that removing senescent cells can restore body functioning in experimental animals. However, the cause of cell senescence in the human body remains a contentious issue.
“The gene expression profile and bioinformatics suggested that cell membrane damage explains the origin of senescent cells in our bodies, specifically the ones near damaged tissues,” Professor Kono said.
Repeated cell division is the most well-documented cause of cellular senescence. Many other stressors, such as DNA damage, oncogene activation, and epigenetic alterations, can cause cellular senescence in a laboratory context. The long-standing dogma in the scientific field was that diverse stimuli eventually cause cellular senescence by activating the DNA damage response.
However, the authors discovered that cell membrane injury causes cellular senescence through a distinct process involving calcium ions and the tumor suppressor gene p53. These findings may help to establish a strategy for achieving healthy longevity in the future.
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