Pcbp2 Regulates P16^Ink4A-Dependent Cellular Senescence In Response To Iron

A recent study reveals that a protein called PCBP2 controls how cells age and stop dividing, a process known as cellular senescence, in response to iron levels in the body, suggesting a link between iron and age-related diseases like atherosclerosis.

Our bodies are constantly working to maintain health, but as we age, our cells can undergo a process called senescence, where they stop dividing and can contribute to various age-related diseases, including heart conditions like atherosclerosis. A new discovery sheds light on a key player in this process: a protein known as PCBP2.

Researchers found that PCBP2 plays a crucial role in regulating cellular senescence. It does this by influencing another important protein, p16INK4a, which is a well-known marker of cellular aging. Interestingly, PCBP2 also controls the activity of CD40, a protein involved in inflammation and the release of signaling molecules that contribute to aging, known as the senescence-associated secretory phenotype (SASP).

What makes this finding particularly significant is the connection to iron. The study revealed that iron, an essential mineral in our bodies, can actually trigger cellular senescence. It does so by working through PCBP2, affecting both p16INK4a and the CD40-mediated SASP. This means that the amount of iron in our cells can directly influence how quickly they age and contribute to disease.

Further experiments showed that reducing the amount of iron inside cells could suppress cellular senescence. Conversely, increasing PCBP2 levels brought back the signs of aging, even in cells with reduced iron. These findings suggest that iron might be an environmental factor that contributes to cellular aging and diseases like atherosclerosis by modulating the activity of PCBP2 and its downstream targets. Understanding this pathway could open new avenues for therapeutic interventions to combat age-related conditions.

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Source: link to paper