Scientists at Duke-NUS Medical School have identified a specific protein, interleukin-11 (IL-11), which increases with age and actively promotes aging. By blocking IL-11, researchers believe they can not only extend lifespan but also mitigate age-related physical decline. Prior studies by the team explored IL-11’s role in heart, kidney, liver, and lung health, leading to an anti-IL-11 therapy currently in clinical trials for fibrotic lung disease.
The latest research builds on these findings, showing that IL-11 contributes to fat accumulation, muscle loss, and reduced strength, all hallmarks of aging. Blocking IL-11 expression in a preclinical mouse model protected against these signs of aging and extended lifespan by about 25%.
Treated mice exhibited increased metabolism, producing beneficial brown fat instead of harmful white fat, retained muscle mass and strength, and were shielded from multiple age-related diseases, including cancer.
The findings highlight a disparity between life expectancy and healthy living years. Professor Thomas Coffman, Dean of Duke-NUS, emphasized the potential of this discovery to enable older adults to live healthier lives longer, reducing frailty and cardiometabolic risks.
The study also noted the broader benefits of inhibiting IL-11, such as reducing telomere shortening and maintaining mitochondrial function, both crucial for cell health. While anti-IL-11 therapy is showing promise in early fibrotic lung disease trials, researchers face challenges in drug approval pathways and funding for aging treatments. Nonetheless, they are optimistic about its potential, estimating that extending healthy lifespan by even one year could be valued at $38 trillion.