Our lab is interested in a simple but ambitious question: how does the genome change with age, and can those changes be understood well enough to reverse them?

We work at the intersection of spatial genomics, epigenetics, and aging biology. Our research has three connected goals. First, we develop new spatial genomics tools to study the genome and transcriptome directly inside cells and tissues, at the nanoscale. Second, we use these tools, together with single-cell genomics approaches, to understand how chronic inflammation reshapes the epigenome during aging and contributes to age-associated disease. Third, we explore whether those changes can be repaired through targeted epigenetic interventions, including CRISPR-based genome editing and epigenetic reprogramming.

At the heart of the lab is the idea that aging is not only a matter of cellular damage, but also of altered epigenomic memory. By studying genome organization and gene regulation in their native spatial context, we hope to understand how inflammatory and aging-related signals become embedded in the genome over time, and how that process might be reversed. Our long-term goal is to build a framework for making the genome more resilient to inflammation, aging, and age-related disease.