And can we understand those changes well enough to reverse them?
We study this question at the intersection of spatial genomics, epigenetics, and aging biology.
We develop spatial genomics tools to study the genome and transcriptome directly inside cells and tissues, at the nanoscale.
Using these tools alongside single-cell genomics, we investigate how chronic inflammation reshapes the epigenome during aging and contributes to age-associated disease.
We test targeted epigenetic interventions, including CRISPR-based genome editing and epigenetic reprogramming, to explore whether harmful changes can be reversed.
Aging involves not only cellular damage, but also changes in epigenomic memory. By studying genome organization and gene regulation in their native spatial context, we aim 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.