Dynamic tissue-specific modulation of redox stress and its impact on health and disease.

Chronic oxidative stress is implicated in a wide range of human diseases, yet its causal and tissue-specific roles in disease initiation and progression remain poorly defined. In this seminar, I will present how redox stress functions as a context-dependent driver of pathology across neurovascular, cardiovascular, maternal (preeclampsia), and metabolic(diabetes) disease states.

I will begin by describing work that uncovered fundamental redox cues guiding neuro-cardiac development. By integrating redox biochemistry with developmental biology, I identified glutathione-dependent oxidants as regulators of calcium signaling that coordinate early brain–heart formation, revealing oxidative molecules as essential developmental signals rather than purely damaging agents.

The second part of the talk focuses on redox-driven mechanisms underlying adult neurovascular and cardiovascular pathology. I will present a chemogenetic, CRISPR-engineered mouse model developed to induce oxidative stress with cell-type precision, demonstrating that neurovascular oxidative injury alone is sufficient to cause sensory ataxia, neurodegeneration, mitochondrial dysfunction, and cardiac hypertrophy. I will also highlight ongoing work in hypertensive disorders of pregnancy, particularly preeclampsia, examining how disrupted redox balance impairs maternal vascular signaling and placental function.

Finally, I will outline my future independent research program investigating how chronic oxidative stress disrupts neuro–islet communication to drive metabolic disease. Planned studies will examine how vagal sensory neuron injury alters β-cell physiology and glucose homeostasis, with the goal of defining redox-dependent neural control of endocrine function.

Overall, this work defines chronic, tissue-specific redox stress as a unifying mechanism underlying disease progression across multiple organ systems and provides a foundation for future therapeutic strategies targeting redox-dependent signaling with cellular and temporal precision.