We explore a fundamental mystery in metabolism: why do neighbouring cells in the same tissue age and fail at different rates? The answer lies in their local metabolic microenvironment, dynamic gradients of oxygen, nutrients, and metabolites that act as powerful local signals. Using spatial multi-omics, we map these invisible landscapes at single-cell resolution to reveal how they control mitochondrial health, fuel choice, and cellular fate. Our goal is to decode these metabolic niches and learn to reprogram it. By targeting maladaptive microenvironments, we aim to restore metabolic resilience in aging, mitochondrial diseases, and metabolic disorders, moving to precision metabolic repair.
Chronic low ferritin in premenopausal women creates a unique endocrine and metabolic state, separate from overt diseases. This project investigates how it causes persistent metabolic reprogramming or scarring, potentially driving accelerated age-related decline. By integrating human population genetics with experimental models, we aim to uncover the fundamental sex-specific mechanisms by which iron metabolism governs metabolic aging. Our goal is to elucidate how dysregulation in women contributes to distinct aging trajectories and vulnerabilities.
As we age, our blood changes, carrying inflammatory signals and depleted regenerative capacity. This "old" blood damages the cardiovascular system, brain, and metabolism, contributing to heart disease, neurodegeneration, and diabetes. Using multi-omics, we map these changes at molecular resolution to pinpoint the key drivers of blood aging. Our goal is to restore youthful blood function, delaying organ deterioration, enhancing resilience, and extending the health span by treating multiple age-related diseases through a single, systemic lever.