Environmental stressors and lifestyle factors can alter liver function by changing cellular signaling and gene regulation, potentially influencing disease susceptibility across the lifespan and, in some cases, across generations without changing the underlying DNA sequence. This raises a central question:

How do environmental stressors reprogram susceptibility to liver disease? 

Our laboratory is particularly interested in understanding how exposures during sensitive developmental windows alter cellular metabolism, mitochondrial function, and epigenetic regulation, creating persistent changes in disease susceptibility. We investigate how these molecular alterations influence liver health and contribute to interconnected diseases and comorbidities.

We integrate fish models, 2D cell culture, and 3D organoid systems with metabolomics, transcriptomics, epigenomics, molecular biology, and advanced imaging to connect environmental exposures with molecular mechanisms and disease outcomes. 

Ultimately, our goal is to identify how environmental stress becomes biologically embedded and to uncover mechanisms that can be targeted to prevent or reduce environmentally driven disease.