Obesity and its associated complications, including insulin resistance, type 2 diabetes and metabolic dysfunction-associated steatotic liver disease (MASLD), arise from complex changes across multiple cell populations in metabolic tissues. Our previous research demonstrated that liver macrophages can regulate hepatic metabolism through non-inflammatory mechanisms during insulin resistance (Science Translational Medicine, 2020) and revealed distinct human liver macrophage subpopulations with different origins and functions (Nature Metabolism, 2023).

Building on these discoveries, our research now investigates diverse immune, stromal, vascular and metabolically active cell populations across the liver and adipose tissue, together with circulating immune cells. We integrate single-cell, spatial and multi-omics technologies with our data-driven approaches to define disease-associated cell states, intercellular communication and molecular regulatory networks. A particular focus is understanding how RNA regulation, such as alternative splicing and RNA editing, shapes cell-state transitions, metabolic stress responses and tissue remodeling during disease progression. By connecting these molecular mechanisms with clinical phenotypes, we aim to identify biomarkers and therapeutic targets for obesity-associated metabolic diseases.