Stress is not only a psychological experience, but a coordinated biological response that integrates neural, vascular, immune, and metabolic systems. These interactions determine how organisms adapt to environmental and physiological challenges.
The vagus nerve serves as a critical communication highway linking the brain to peripheral organs, including the pancreas, heart, and gut. Through vagal sensory afferents, these organs continuously relay information about their metabolic and physiological state to the central nervous system, enabling rapid, coordinated regulation of glucose homeostasis, cardiac function, and gut physiology.
Our research investigates how oxidative stress disrupts this vagal communication network, with a focus on interactions between pancreatic beta cells, the heart, and the gut. We aim to understand how redox imbalance alters signal transduction within vagal sensory neurons — from receptor-level changes to downstream intracellular signaling cascades — and how these disruptions translate into metabolic dysfunction. By combining approaches spanning chemogenetics, molecular signaling, neural circuit analysis, and systemic metabolic assessment, we seek to define how oxidative stress reshapes gut-brain and cardiac-brain communication, and how this contributes to the progression of metabolic diseases such as diabetes and cardiometabolic disorders.
Ultimately, our goal is to identify the redox-sensitive nodes within vagal sensory circuits that could serve as therapeutic targets for restoring healthy organ-brain communication in metabolic disease.
We study how oxidative stress alters the function of vagal sensory neurons that relay metabolic information from the pancreas, heart, and gut to the brain. A central goal is to identify how redox imbalance disrupts normal signal transduction within these circuits and drives the transition from adaptive organ-brain communication to pathological signaling. By combining molecular signaling analysis with neural circuit approaches, we map how oxidative modifications at the receptor and intracellular level reshape vagal afferent activity and contribute to metabolic disease progression.
We investigate how oxidative stress disrupts communication between pancreatic beta cells and the vagal sensory neurons that monitor their function, contributing to impaired glucose sensing and insulin regulation in diabetes. Our work examines how redox-driven changes at the beta cell–vagal interface alter the fidelity of metabolic signaling to the brain, and whether restoring healthy redox balance at this interface can re-establish normal glucose homeostasis. This research aims to identify specific molecular targets for reversing vagal dysfunction in diabetic states.
We use chemogenetic tools to selectively manipulate redox state within defined neuro-islet circuits, allowing us to causally test how oxidative signaling shapes communication between pancreatic islets and their innervating sensory neurons. By precisely controlling redox activity at specific circuit nodes, we can determine which molecular and cellular changes are sufficient to disrupt — or restore — healthy neuro-islet signaling, providing a platform for identifying targeted redox-based therapeutic strategies.
Our long-term goal is to define fundamental principles of stress biology across scales — from molecular signaling to whole-brain systems — and to translate these insights into strategies that enhance resilience and prevent disease. We believe that mechanistic clarity at each level of biological organization is the prerequisite for developing durable, effective interventions.
