What inspired you to pursue aging research?
Since childhood, I’ve wanted to understand the process of aging and ultimately slow it so people have more time with their loved ones. Later, as an undergraduate, I discovered the joy of research, fell in love with the scientific process, and decided to pursue a PhD in Drosophila chromatin biology. For my postdoc, I chose to focus squarely on aging; age-related chromatin changes felt both promising and understudied. Opportunities to do this work were limited in Russia, so I looked abroad. I changed fields and joined the Gorbunova lab—a calculated move that has allowed me to study mammalian aging, build on SIRT6-centered epigenetic regulation, and work in an environment that encourages translational research. This path pairs my chromatin biology training with a clear purpose: to uncover mechanisms that drive age-related decline and translate them into interventions that extend healthy years.
In your view, what does AFAR mean to the field, and what does it mean, for you, to receive an AFAR grant now?
AFAR is a beacon in aging research—attracting talent, funding bold early work, and connecting basic, translational, and clinical researchers through a trusted network. For me, this award is catalytic: independent funds for my own ideas, credible validation, and entry into a small, influential community. It shifts me from supporting roles to leading roles—with my own budget and milestones—greatly accelerating my path to independence.
What is exciting about your research’s potential impact?
Transcriptional dysregulation is emerging as a major driver of aging, yet no intervention directly targets it.
This project targets a regulatory checkpoint—RNA polymerase II pausing—using low-dose CDK9 inhibitors. Originally developed for cancer, they provide a fast repurposing route to anti-aging intervention. Success will establish Pol II pausing as a therapeutic node and deliver a translationally ready intervention for healthier aging.
How would you describe your research to a non-scientist?
At the start of each gene, cells have a built-in “speed bump” that keeps traffic orderly. At that checkpoint, the cell decides whether to continue or abort reading. With age, this “speed bump” flattens. First, immune signals become noisy. Second, bits of “junk DNA” that should be aborted are read, stressing cells. I test low-dose versions of drugs already tried in cancer to gently restore that speed bump to youthful levels. The goal is to quiet harmful inflammation and keep gene activity on track.
