How do environmental exposures during fetal and early-postnatal life — hypoxia, undernutrition, environmental toxicants, maternal stress — reshape the developing cardiovascular system, and how do those changes lie dormant for decades before manifesting as adult disease?
The Goyal Laboratory approaches this question at three levels. At the molecular level, we map the epigenetic modifications — DNA methylation, histone marks, non-coding RNAs — that translate transient exposures into persistent transcriptional programs. At the tissue level, we characterize the resulting changes in vascular reactivity, contractile protein expression, and endothelial function across the maternal and fetal circulations. At the systems level, we use computational physiology and digital-twin modeling to predict how molecular-level perturbations cascade into clinically observable phenotypes.
This integrated approach is designed to identify intervention windows — moments in development when a modifiable exposure could redirect disease trajectory. The end goal is translational: tools clinicians can use to screen, stratify, and intervene before silent biology becomes overt disease.