The evolution of cellular senescence is a remarkable question. It connects to development, organismal life-span, protection against cancer, and its rate seems to vary between species. Moreover, since life-span of the cell is inherently linked to how much external stress it gets exposed to, the rate of cellular aging determines the ecology of the cell (e.g., how much oxidative stress the cell got exposed to). Of course, there are other fascinating angles, such as the effect of somatic mutations and telomere length in this process.
We had an opportunity to work on this problem with the excellent Atilla Group at UB, who have been interested in the changes in lipidome during cellular senescence. Our first collaborative paper showed that indeed specific lipids (which are highly regulated) are major players in the process of cellular aging. Now, my postdoc Marie led a study where we combined some evolutionary insights with a rigorous analysis of the transcriptome changes during cellular aging. One gene, CD36, light up like a Christmas light. We found that this gene is a fundamental player in cellular aging, and in fact when we induced its expression in young cells, it leads to rapid cellular senescence.
One really cool aspect of this gene is that it plays an important role as a target for the malaria parasite Plasmodium. As such, we have an unexpected pleiotropic effect where it is plausible that resistance/susceptibility to infectious disease may be related to cellular senescence – and by proxy organismal aging. It is very very exciting and I cannot wait to see what is going to be revealed in the coming years.