Toxicology & Pharmacology

Research Strategy

The Gölz Lab investigates how environmental chemicals—including per- and polyfluoroalkyl substances (PFAS)—perturb intracellular signaling networks and how these early molecular events propagate across biological scales to drive functional tissue changes and organismal phenotypes. Guided by a One Health perspective, we connect environmental exposure to mechanistic pathways relevant for human and ecosystem health. We integrate human iPSC-derived 2D systems, such as advanced 3D organoid models, and zebrafish embryo assays to dissect conserved pathways and derive mechanistic, dose-resolved effect chains.

In human cardiac platforms (iPSC-derived cardiomyocytes and 3D cardiac organoids), we quantify effects on key Ca²⁺-signaling control points, cellular stress responses, and pro-fibrotic remodeling. By combining functional phenotyping (contractility and Ca²⁺ handling) with molecular profiling, we link PFAS-related pathway perturbations to clinically relevant outcomes including arrhythmogenic risk, hypertrophy, and fibrosis-associated phenotypes.

Complementary zebrafish embryo assays enable high-content imaging and quantitative in vivo phenotyping of cardiac and developmental endpoints, supporting cross-vertebrate comparison and scalable testing. A core goal of the lab is cross-scale integration and modeling—spanning adverse outcome pathway (AOP) development and data-driven frameworks—to move beyond isolated endpoints toward predictive, mechanistically grounded New Approach Methodologies (NAMs) that increase human relevance, strengthen environmental and pharmacological decision-making, and support 3R-aligned reduction of animal-intensive testing.

We develop and validate New Approach Methodologies (NAMs) to understand chemical effects mechanistically and improve human relevance while supporting the 3R principle. Our work combines zebrafish embryo assays with human iPSC-derived 2D and 3D models, including 3D human heart organoid -based systems. We integrate molecular and functional readouts to build causal effect chains from early molecular perturbations to tissue- and organism-level outcomes such as thyroid disruption in fish and arrhythmogenesis, hypertrophy and fibrotic remodeling in human cardiac models.