Role of mitochondrial reactive oxygen species for triggering inflammation during cardiac pressure overload (B04)

• Subject Area: Cardiology, Angiology
• Term: since 2022
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 453989101

Mitochondria are the main source for energy, but also for reactive oxygen species (ROS) in the heart. An increase in hemodynamic load, which can be cause and consequence of heart failure, drains reducing equivalents in mitochondria towards ATP production at the cost of the antioxidative capacity, and the ensuing excessive ROS emission triggers cardiac remodeling and dysfunction. Here, we address how cardiomyocyte mitochondria relay increased hemodynamic load to activation of the inflammasome and vice versa, how cardiac inflammation compromises cardiomyocyte excitation-contraction coupling and mitochondrial energetics.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1525: Cardio-Immune Interfaces
• Applicant Institution: Julius-Maximilians-Universität Würzburg
• Project Head: Professor Dr. Christoph Maack