Adipocyte Communication and Tissue Homeostasis

Adipose tissue is a dynamic endocrine and immunological organ that continuously communicates with neighboring cells and distant metabolic tissues. This communication is mediated by a complex network of secreted proteins, proteolytic enzymes, extracellular matrix remodeling, receptor signaling, and intracellular regulatory pathways that together maintain adipose tissue homeostasis. In obesity, these communication networks become disrupted, resulting in chronic inflammation, impaired metabolic function, insulin resistance, and reduced thermogenic capacity.

Our research aims to understand the molecular mechanisms that coordinate adipocyte communication in health and disease. We investigate how adipokines, serpins, proteases and other protein regulators shape interactions between adipocytes, immune cells, vascular cells and the extracellular matrix. Using complementary approaches ranging from recombinant protein biochemistry and structural studies to primary human adipocytes, mouse models and multi-omics analyses, we identify signaling pathways that regulate inflammation, lipid metabolism and tissue remodeling.

Particular emphasis is placed on multifunctional protein regulators whose activities extend beyond their classical roles. Our work has uncovered unexpected mechanisms through which proteins such as the serpin vaspin and kallikrein proteases influence adipocyte biology, immune cell recruitment, thermogenic function and metabolic homeostasis. By defining these communication networks at molecular resolution, we aim to identify novel therapeutic strategies that preserve healthy adipose tissue function and prevent obesity-associated metabolic disease.

Our goal is to define the protein networks that coordinate adipose tissue communication and to exploit these pathways to prevent inflammation and metabolic dysfunction.