'Mitochondrial communication is key' Cross-compartmental signals maintaining proteostasis and longevity

Aging is a complex biological phenomenon. Better understanding of underlying mechanisms of aging promotes development of preventative therapies for chronic, degenerative age-related diseases such as type 2 diabetes, obesity, cardiovascular disease, cancer and Alzheimer's disease. While aging has long been considered a passive process, evidence has accumulated in model organisms that targeting specific cellular pathways strongly affects health and longevity. This thesis presents insights into the cellular processes related to aging, with an underlying quest for understanding how cellular cross-compartmental signals ensure longevity.
Mitochondria are the compartments responsible for producing energy in the cell. While mitochondria produce energy, one of the processes in the cell that consumes most energy is translation of mRNA into protein carried out by ribosomes. In this thesis we show how mitochondrial communication and metabolism can regulate the aging process. For instance by slowing down protein synthesis. Using less energy by slowing down mitochondria, and simultaneously synthesizing less new proteins by having less ribosomes, leads to a more sustainable state of the cell overall. To maintain sustainability, signals are sent, inducing processes such as proteostasis and quality control to ultimately lead to cytoprotection and longevity.
The more we know on the precise mechanisms of mitochondrial compartmental signaling, the more we could exploit these for possible treatments. With the human population getting older, and the last years of life often being accompanied by age-related diseases, therapeutic approaches that could prevent these diseases would have a huge impact.