Research

The MacDougald laboratory focuses broadly on adipose tissue biology and mesenchymal cell fate, with particular emphasis on the molecular and cellular mechanisms underlying lipodystrophy and bone marrow adipose tissue (BMAT). Their work on lipodystrophy centers on familial partial lipodystrophy type 2 (FPLD2), a disorder characterized by selective loss of peripheral adipose tissue caused by pathogenic variants in the LMNA gene encoding nuclear lamins A/C. Using an integrated approach that includes clinical patient samples, adipocyte-specific Lmna knockout and Lmna variant mouse models, and complementary cell culture systems, the lab is defining how lamin A/C dysfunction perturbs lipid metabolism, mitochondrial function, inflammatory signaling, and adipocyte survival, providing translational insight across human, mouse, and cellular models. In parallel, the lab has been a pioneer in the study of BMAT, a distinct adipocyte depot with important roles in bone biology and systemic metabolism. To interrogate bone marrow adipocyte function with precision, they have developed novel mouse models enabling recombination specifically in marrow adipocytes, allowing targeted manipulation of genes such as Pnpla2 and rigorous assessment of how marrow adipocytes regulate the marrow niche, including hematopoiesis and bone homeostasis.