加齢：炎症性タンパク質を阻害するとマウスの寿命が延びる

The ageing effects of a pro-inflammatory protein called IL11 in mice are reported in Nature this week. Inhibition of this protein is shown to improve the health of old mice and increase their lifespan. The effects of IL11 inhibition in humans remain to be seen, although early-stage clinical trials are underway to understand the effects of this treatment in patients with fibrotic lung disease.

Biological signalling pathways associated with health and lifespan are often perturbed in old age, with pro-inflammatory signalling being one such outcome implicated in ageing. Anissa Widjaja, Stuart Cook and colleagues investigated how a pro-inflammatory cytokine called IL11 (a signalling protein that mediates inflammation) affects age-associated disease and lifespan in mice. They found that IL11 is upregulated as mice age and show that the increased levels of this cytokine activate signalling pathways associated with ageing.

Following these observations, the authors investigated how interfering with IL11 activity impacts age-associated disease and lifespan in mice. Deleting the gene associated with IL11 expression is shown to protect against metabolic decline, multiple illnesses and frailty in old age, and extended the lives of both sexes by 24.9% on average. Blocking IL11 with an antibody improved metabolism and muscle function while reducing signs of ageing and frailty in both male and female mice. In mice aged 75 weeks (human equivalent of 55 years old), IL11 inhibition increased lifespan by 22.4% in males and 25% in females. Inhibition of IL11 also seems to reduce the incidence of age-related cancer, a notion that has previously been suggested.

Together the findings show that anti-IL11 therapy can improve health and extend lifespan in ageing animals; whether this applies to humans requires further investigation.