We investigate how early-life exposure to environmental stressors programs susceptibility to liver disease. Our work examines endocrine-disrupting chemicals and other physical stressors that can alter developmental pathways and increase the risk of adult liver disease.

We focus on the molecular mechanisms that link early childhood exposure to long-term adult diseases, including mitochondrial stress, disrupted energy metabolism, oxidative stress, altered hormonal signaling, and epigenetic dysregulation. By integrating environmental toxicology, molecular biology, and systems-level approaches, we seek to identify early biological changes that predict disease risk and reveal opportunities for prevention.

When environmental stressors disrupt liver function, the consequences can extend well beyond the liver, reshaping whole-body metabolism and increasing susceptibility to chronic disease. We are interested in investigating how these early hepatic disturbances are transmitted to distant organs through circulating metabolites, inflammatory signals, hormones, and extracellular vesicles.

By combining in vitro and in vivo models, we aim to uncover how a stressed liver becomes a driver of systemic metabolic and reproductive dysfunction. Ultimately, our goal is to identify early biomarkers and actionable therapeutic targets that can interrupt the progression from environmentally induced liver injury to systemic metabolic disease. 

Our organoid research program develops physiologically relevant three-dimensional liver and intestinal models to study how environmental exposures disrupt tissue health, metabolism, and disease susceptibility. These models preserve key cellular, structural, and functional properties of native tissues, allowing us to examine toxicant effects in a controlled and biologically meaningful setting.

We use organoids to evaluate exposure-driven changes in tissue architecture, cell viability, lipid metabolism, mitochondrial function, oxidative stress, inflammation, and regenerative capacity. We will integrate CRISPR–dCas9 epigenome editing with organoid models to determine how exposure-associated changes in gene regulation contribute to metabolic dysfunction. Targeted editing of DNA methylation and chromatin activity allows us to test causal pathways and identify reversible molecular targets involved in tissue injury.