Areas of Interest

Metabolic disease and adipose tissue dysfunction

A major focus of the lab is understanding how adipose tissue dysfunction contributes to obesity, aging, and systemic metabolic decline. Rather than viewing adipose tissue solely as an energy storage site, we study how loss of regulatory control within adipose tissue leads to impaired tissue function and downstream metabolic consequences. Our work aims to identify the mechanisms that drive adipose tissue failure and their relevance to whole-body metabolism.

Vascular adipocyte progenitor cell niches

We are particularly interested in how adipocyte progenitor cells are regulated within specialized vascular niches. These niches provide critical signals that control progenitor cell fate, tissue maintenance, and regenerative capacity. Our studies define how vascular environments shape adipocyte formation and how disruption of these niches alters adipose tissue structure and function in obesity and aging.

Adipose tissue plasticity across the lifespan

Adipose tissue must continuously adapt during development and in response to physiological and metabolic challenges. We investigate how adipose tissue plasticity is regulated across the lifespan and how adaptive capacity is progressively lost with aging and metabolic stress. By defining when and how these processes fail, we aim to identify principles that govern tissue resilience and vulnerability.

Genetic control of adipose tissue remodeling

We use genetic models to dissect the molecular and cellular pathways that regulate adipose tissue remodeling, including tissue growth, maintenance, and thermogenic capacity. These approaches allow us to define causal mechanisms that distinguish healthy adipose tissue adaptation from pathological remodeling in metabolic disease.

Inter-tissue communication in metabolic health

Adipose tissue function is shaped by signals from other metabolic tissues, including muscle, immune, and vascular systems. We examine how inter-tissue communication coordinates adipose tissue behavior and how disruption of these signaling networks contributes to metabolic dysfunction. This systems-level perspective connects cellular mechanisms within adipose tissue to organism-wide metabolic outcomes.