Good news! More on the fountain of youth! This could be a breakthrough!
"... In a new paper appearing in Nature, the team demonstrated in preclinical mouse studies that the protein interleukin-11 (IL11) actively promotes aging, and that giving an anti-IL11 therapy not only counteracts the deleterious effects of aging but also increases lifespan. ...
When more IL11 was produced by these organs, it promoted fat accumulation in the liver and abdomen, and reduced muscle mass and strength — two conditions that are hallmarks of human aging. ...
demonstrated that by applying this anti-IL11 therapy in the same preclinical model, metabolism was improved. The mice shifted from generating white fat to beneficial brown fat. ...
demonstrated that by applying this anti-IL11 therapy in the same preclinical model, metabolism was improved. The mice shifted from generating white fat to beneficial brown fat. ...
The researchers also observed improved muscle function and overall better health in their study, as well as an increased lifespan by up to 5 per cent in both sexes. ...
also reduced the rate of telomere shortening and preserved mitochondria’s health and ability to generate energy. ..."
also reduced the rate of telomere shortening and preserved mitochondria’s health and ability to generate energy. ..."
From the abstract:
"For healthspan and lifespan, ERK, AMPK and mTORC1 represent critical pathways and inflammation is a centrally important hallmark. Here we examined whether IL-11, a pro-inflammatory cytokine of the IL-6 family, has a negative effect on age-associated disease and lifespan. As mice age, IL-11 is upregulated across cell types and tissues to regulate an ERK–AMPK–mTORC1 axis to modulate cellular, tissue- and organismal-level ageing pathologies. Deletion of Il11 or Il11ra1 protects against metabolic decline, multi-morbidity and frailty in old age. Administration of anti-IL-11 to 75-week-old mice for 25 weeks improves metabolism and muscle function, and reduces ageing biomarkers and frailty across sexes. In lifespan studies, genetic deletion of Il11 extended the lives of mice of both sexes, by 24.9% on average. Treatment with anti-IL-11 from 75 weeks of age until death extends the median lifespan of male mice by 22.5% and of female mice by 25%. Together, these results demonstrate a role for the pro-inflammatory factor IL-11 in mammalian healthspan and lifespan. We suggest that anti-IL-11 therapy, which is currently in early-stage clinical trials for fibrotic lung disease, may provide a translational opportunity to determine the effects of IL-11 inhibition on ageing pathologies in older people."
Fig. 1: The IL-11–ERK–mTORC1 signalling module is upregulated in ageing and associated with senescence and metabolic decline.
Fig. 2: Female Il11-deleted mice are protected from age-associated obesity, frailty, and metabolic decline.
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