Human aging is a complex process driving the progressive decline of homeostasis and the regenerative potential of tissues. Senescent cells accumulate and compromise the function of organs, contributing to various age-related diseases. Disturbed mitochondrial function, inter-organelle communication, proteostasis, and metabolic control lead to senescence-associated dysfunctions. However, the underlying mechanisms are still largely unexplored.We hypothesize that unveiling age-related alterations in mitochondrial function, inter-organelle communication, and proteostasis will facilitate the identification of novel mechanisms and regulatory pathways driving cellular senescence. Based on our findings, we aim to develop and characterize new small molecules that target core components driving cellular senescence.

To understand how disturbed mitochondrial function, inter-organelle communication, proteostasis, and metabolic control synergize to drive cellular senescence, the consortium will join forces to unravel underlying mechanisms in an unprecedented interdisciplinary approach, using various in vitro aging models, genetically engineered strains of Saccharomyces cerevisiae and Caenorhabditis elegans, along with mice and human organoids. As a major innovative aspect, we aim to identify novel small molecules with anti-senescence properties based on results from in vitro and in vivo models.

In this project, my research group will join forces with Prof. Dr. Pidder Jansen-Dürr and Dr. Teresa Kaserer from the University of Innsbruck and will Markus Schosserer from the Medical University of Graz. Within my group, a PhD. student and a technician will elaborate on this project to unveil novel mechanisms of senescence and molecular components suitable to serve as targets for delaying the progression of senescence.