When cells become damaged beyond repair, our bodies have a mechanism for eliminating them: a process known as apoptosis, or programmed cell death. Occasionally, however, damaged cells evade apoptosis and instead enter a state called cellular senescence. Senescence is an important tumour-suppressive mechanism that prevents damaged cells that evade apoptosis from continuing to divide and potentially developing into cancer.

Senescent cells stop dividing, but they don't die. Instead, they remain metabolically active and begin secreting signalling molecules that the immune system uses to find the cells and clear them. As we age, our immune system itself deteriorates, becoming worse at clearing senescent cells. They accumulate, and the molecules they release cause chronic inflammation in the surrounding tissue, accellerating aging. This raises an intriguing question: could we slow down aging by selectively eliminating the senescent cells that accumulate later in life?

In this conversation, I speak with Paul Robbins, who was part of the research team involved in identifying the first drugs capable of selectively targeting and eliminating senescent cells. These drugs are known as senolytics. Studies in mice have produced promising results, showing improved health and longevity, with extensions in lifespan of up to 15%. The central question of this conversation is whether these results might transfer to humans.

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