Elucidating the pathomechanisms of compromised fracture healing in osteoporosis: Consequences of mitochondrial dysfunction (B09* (C01))

• Subject Area: Orthopaedics, Traumatology, Reconstructive Surgery
• Term: since 2023
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 251293561

In the 2nd funding period, we discovered for the first time that bone-resident mast cells contribute to trauma-induced impaired fracture healing by influencing systemic and local immune responses after injury. They are also crucially involved in compromised fracture healing caused by osteoporosis and stimulate osteoclastogenesis by releasing osteoclastogenic mediators, including Midkine and CXCL10, in an estrogen-dependent manner. We will further focus on impaired osteoporotic bone healing in the 3rd funding period, and determine the impact of mitochondrial dysfunction and disturbed ROS homeostasis on the function and fate of osteoblasts and chondrocytes during fracture healing.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1149: Danger Response, Disturbance Factors and Regenerative Potential after Acute Trauma
• Applicant Institution: Universität Ulm
• Project Heads: Professorin Dr. Anita Ignatius; Dr. Jana Riegger-Koch