Bone repair following fracture is a tightly regulated process in which early inflammatory responses determine the outcome of tissue regeneration. However, the signals that control metabolic reprogramming of immune cells during bone healing, and how aging disrupts these mechanisms, remain poorly understood.

In this project, we investigate how communication between innate and adaptive immune cells shapes metabolic adaptations during the early inflammatory phase of bone repair. In particular, we focus on signaling pathways governing monocyte–T cell interactions and how aging alters immune sensing of tissue damage and repair.

By integrating single-cell and multi-omic analyses with mouse fracture models and human patient samples, we map immune cell states and the signaling networks that control their metabolic reprogramming. These insights aim to identify therapeutic targets to improve bone healing in patients with impaired regenerative capacity.