Senescence-Inhibitory Δ133P53Α Counteracts Accelerated Ageing And Mortality
Scientists have identified a naturally occurring variant of a well-known protein, called Δ133p53α, that shows promise in combating the effects of aging. This variant acts by putting the brakes on a process called cellular senescence, where cells stop dividing and can release harmful substances, contributing to aging and age-related diseases. In laboratory studies using cells from patients with Hutchinson-Gilford progeria syndrome, a condition causing accelerated aging, Δ133p53α was found to reduce cellular aging, decrease inflammation, and protect against DNA damage.
Further research in a mouse model of this premature aging syndrome demonstrated that increasing the levels of Δ133p53α throughout the body not only replicated these beneficial cellular effects but also extended the animals’ median lifespan by 11%. The protein variant helped maintain the health and structure of vital tissues like the aorta and skin, preventing the typical age-related damage seen in these mice. These findings suggest that Δ133p53α may activate a wide range of mechanisms that fight aging, including improving bone health, metabolism, antioxidant defenses, and even maintaining the youthful state of our genetic material and stem cells.
This discovery opens up exciting possibilities for developing new treatments, not just for rare conditions like progeria, but potentially for broader strategies to prevent or delay the aging process in the general population. The unique ability of Δ133p53α to selectively inhibit harmful cellular aging while preserving important DNA repair functions makes it a particularly intriguing target for future therapeutic interventions.
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