NEW INSIGHTS INTO MITOCHONDRIA AND CELLULAR SENESCENCE

Abstract Senescence(definition) is a multi-functional cell fate, characterized by an irreversible cell-cycle arrest and a pro-inflammatory phenotype, commonly known as the senescence-associated secretory phenotype (SASP). Emerging evidence indicates that accumulation of senescent cells in multiple tissues drives tissue dysfunction and several age-related conditions. This has spurred the academic community and industry to identify new therapeutic interventions targeting this process. Senescence is a complex and highly heterogenous phenotype and despite tremendous progress in recent years we are still far from fully understanding it. There is no single, stand-alone marker that allows the identification of senescent cells, posing a challenge to their identification and targeting. Mitochondrial dysfunction(definition) is an often-unappreciated hallmark of cellular senescence which plays important roles not only in the senescence growth arrest but also in the development of the SASP and resistance to cell-death. In my talk, I will first describe some of our recent efforts to accurately map senescent cells in different tissues during aging. Additionally, I will describe how mitochondria contribute to the development of senescence and resistance to cell-death. Finally, I will propose that a detailed road map of mitochondrial biology in senescence will be crucial to guide the future development of therapies targeting cellular aging.