Researches cellular senescence in the heart and kidney during aging through characterization of genetic influences that contribute to senescence-associated secretory phenotypes.
I research the genetic impacts of cellular senescence in the aging process, utilizing diversity outbred mice as a model for human aging. Cellular senescence refers to the state where cells permanently cease dividing and become resistant to apoptosis. In the context of aging, senescent cells can adopt a senescence-associated secretory phenotype (SASP), triggering heightened inflammatory signaling that can result in chronic inflammation, a key factor in various age-related diseases. My objective is to uncover the genetic determinants driving senescence during aging and evaluate the optimal utilization of senolytic drugs. My expertise in cell biology, omics, and circadian biology equips me to address this research challenge using tissue-based assays, omics datasets, and cellular assays. My former training is a Bachelor of Science in Biology from the University of North Texas (’18), followed by a Doctorate of Philosophy in Biology from Rensselaer Polytechnic Institute (’23).