A mechanism by which chronic low-grade inflammation may lead to cell senescence and ageing in mice has been reported in this week’s Nature Communications.
Chronic inflammation is associated with both normal and pathological ageing. Telomere damage, resulting in cellular senescence-living cells that no longer grow or divide-limits the ability of tissue to regenerate and repair itself, an ability which is of prime importance for maintaining organ function during ageing.
Thomas von Zglinicki and colleagues show that chronic, progressive low grade inflammation, in genetically modified mice, induces premature ageing. They hypothesize that this is due to enhanced telomere shortening due to DNA damage from reactive oxygen species-chemically reactive molecules containing oxygen-and that this in turn accelerates the accumulation of senescent cells. Cell senescence then aggravates chronic inflammation, limits tissue regeneration and further accelerates ageing. Researchers also found that accumulation of senescent cells in affected tissues was blocked by treatment with the anti-inflammatory drug ibuprofen or with antioxidants, which rescues the tissues’ ability to regenerate.
These data indicate that inflammation can accelerate ageing in the absence of any other genetic or environmental factor. However, the molecular and cellular mechanisms of these interactions during ageing are not completely understood. In addition, the type of genetic modification used to induce aging in mice is accompanied by severe pathologies. The relevance of these observations to normal ageing, and ageing in humans, therefore remains somewhat uncertain.