Characterizing Senescence Regulators Encoded in the Mitochondrial Genome
As we age, our cell’s ability to cope with changes worsens, making it difficult to maintain a healthy state. Cellular senescence, a cellular state akin to a “life-sentence” whereby cells are permanently locked down from dividing, is strongly implicated in a wide spectrum of age-related diseases. There has been much interest garnering in the development of drugs to target cellular senescence for the prevention and treatment of age-related diseases. Senescence is known to be regulated by a multitude of factors that are encoded in our nuclear genome. However, our cells keep two genomes in separate areas, the nucleus and mitochondria, which each have genes that actively communicate with each other to keep our cells healthy. We are exploring how mitochondria send messages to communicate with the nucleus and how this process changes during aging. I am specifically focusing on a novel peptide that are inherently encoded in the mitochondrial genome. My research aims to unveil how this novel peptide regulate cellular senescence that will pave the way to identifying new therapies to target senescence. This project will provide the new concept that cellular senescence, and ultimately aging, is regulated not only by genes encoded in the nuclear genome, but also the mitochondrial genome. This would provide a whole new layer to our understanding of how we age and therefore open unexplored doors to new therapeutic targets for age-related maladies.